hepatitis essay conclusion

Eliminating the Public Health Problem of Hepatitis B and C in the United States: Phase One Report (2016)

Chapter: 4 conclusion, 4 conclusion.

Hepatitis B and C kill about 20,000 people every year in the United States, and more than 1 million worldwide ( CDC, 2013 ; WHO, 2016 ). Hepatitis B virus (HBV) and hepatitis C virus (HCV) together account for most viral hepatitis, which kills more people every year than road traffic injuries, HIV and AIDS, and diabetes ( WHO, 2016 ). While the deaths from other common killers (i.e., malaria, tuberculosis, and HIV) have decreased since the early 2000s, deaths attributable to viral hepatitis continue to rise ( IHME, 2016 ).

These deaths can be averted. Three doses of HBV vaccine convey 95 percent immunity ( WHO, 2015 ). Though HBV infection cannot be cured, proper treatment can reduce viral load to an undetectable level ( EASL, 2012 ). While there is no vaccine for HCV, new curative treatments can eliminate the infection in over 95 percent of patients ( Afdhal et al., 2014 ; Charlton et al., 2015 ; Feld et al., 2014 ). Improved prevention and expanded access to viral hepatitis treatments could greatly reduce the burden of these infections. The World Health Organization (WHO) estimates that reducing the incidence of chronic hepatitis B and C by 90 percent and reducing mortality by 65 percent would save 7.1 million lives by 2030 ( WHO, 2016 ).

The United States has an opportunity and a responsibility to be part of the global action against hepatitis B and C. Already the Department of Health and Human Services’ viral hepatitis action plan lays out ambitious goals for improving prevention and care, and expanding hepatitis surveillance ( HHS, 2014 ). In the near term, the committee finds control of both diseases to be imminently possible. This committee also believes that a more ambitious goal is within our reach: Elimination of HBV and HCV as

public health problems in the United States. Although an elimination goal is entirely feasible, it is not necessarily likely without considerable attention to the barriers discussed in this report. First of all, disease reductions programs require an accurate understanding of the true burden of disease in a population. There is wide uncertainty in all estimates of HBV and HCV incidence and prevalence. Limited surveillance contributes to the uncertainty, as does the often asymptomatic course of the infections. Wider screening could help identify more chronically infected people, but screening for both infections is complicated.

Expanding screening for chronic HBV and HCV infections would surely identify new cases, but some would be among people with no access to care. Diagnosis with a chronic disease requires follow-up in primary care. Diagnosis of chronic hepatitis B carries with it the opportunity for treatment and monitoring to reduce the long-term risk of liver cancer and cirrhosis. It also offers the opportunity to vaccinate the patient’s uninfected contacts. Such follow-up is not an option for people who are uninsured and ineligible for Medicaid.

Hepatitis B and C care require a health workforce knowledgeable about long-term management of viral hepatitis. Much of the burden falls on primary care providers, who are already overworked, and extends indefinitely. There is no cure for hepatitis B, and infected individuals require management for the rest of their lives. Hepatitis C, in contrast, can be cured in 8 to 12 weeks, thanks to new direct-acting antiviral drugs. These drugs are expensive in the United States. The first of these treatments to gain Food and Drug Administration approval cost $1,000 per pill in 2014 ( Sanger-Katz, 2014 ). Competition from other products has brought the price down, but curing a chronically infected HCV patient in the United States still costs between $54,000 and $168,000 ( Bickerstaff, 2015 ; Loria, 2016 ). Even at such prices, curing hepatitis C is cost-effective ( Bickerstaff, 2015 ; Chhatwal et al., 2015 ; Najafzadeh et al., 2015 ; Younossi et al., 2015 ). The tension between the expense and cost-effectiveness of treating HCV puts Medicaid and insurance companies in a difficult position. They have responded by restricting access to treatment to only the sickest HCV patients. Even so, HCV treatments alone accounted for about a third of the sharp acceleration in drug spending between 2013 and 2014 ( Martin et al., 2015 ). It is currently not financially possible to treat all the estimated 2.7 to 4.7 million people thought to have chronic HCV infection given the current prices ( Edlin et al., 2015 ; Ward and Mermin, 2015 ).

The high price of treatment creates a tension in determining which patients’ treatment should be a priority. Those at most immediate risk of death are not necessarily those transmitting the virus, so the goals of ending HCV transmission and ending deaths from hepatitis C are somewhat at odds with each other.

There are creative strategies to mitigate this and other barriers to eliminating hepatitis B and C. Five years ago curing HCV infection with short-term, tolerable therapy seemed impossible. Similar breakthroughs in the treatment and management of hepatitis B are possible, as is the development of a prophylactic vaccine for HCV. This report has identified no shortage of research questions for basic scientists, pharmaceutical companies, and health services researchers. None of these questions is especially new, however. The challenge of directing more research interest to viral hepatitis remains.

It is also possible that limitations in disease surveillance, screening, treatment, vaccination, and research are all consequences of a more basic problem. Viral hepatitis is not a public priority in the United States. This too could change; attitudes toward disease can shift rapidly. Education and successful elimination of HBV among Alaskan Natives accompanied changes in local attitudes toward the disease. Liver disease often carries a stigma, perhaps because of its association with drug and alcohol use and sex; HBV and HCV can cause particular shame and distress in patients. Stigma, in turn, encourages silence and inaction among infected people, which is antithetical to any elimination program.

In making its conclusion regarding the feasibility of hepatitis B and C elimination, the committee acknowledges that considerable barriers must be overcome to meet these goals. For example, as elimination policies gain traction, the risk of infection should fall. Some people may respond by reducing efforts to protect themselves from infection. Public health campaigns highlighting the importance of elimination and the need to prevent individual infection might mitigate such behavior. A discussion of this and other solutions to the problems discussed in this report is not within the scope of the project. A second report, to be released in 2017, will outline a national strategy to eliminate hepatitis B and C. This report will discuss ways to address the critical factors and reduce the barriers to elimination set out in this document. The second phase of this project will also explore specific national targets for the elimination effort.

Afdhal, N., S. Zeuzem, P. Kwo, M. Chojkier, N. Gitlin, M. Puoti, M. Romero-Gomez, J. P. Zarski, K. Agarwal, P. Buggisch, G. R. Foster, N. Brau, M. Buti, I. M. Jacobson, G. M. Subramanian, X. Ding, H. Mo, J. C. Yang, P. S. Pang, W. T. Symonds, J. G. McHutchison, A. J. Muir, A. Mangia, P. Marcellin, and I. O. N. Investigators. 2014. Ledipasvir and sofosbuvir for untreated HCV genotype 1 infection. New England Journal of Medicine 370(20):1889-1898.

Bickerstaff, C. 2015. The cost-effectiveness of novel direct acting antiviral agent therapies for the treatment of chronic hepatitis C. Expert Review of Pharmacoeconomics & Outcomes Research 15(5):787-800.

CDC (Centers for Disease Control and Prevention). 2013. Viral hepatitis surveillance: United States, 2013. Atlanta, GA: Centers for Disease Control and Prevention.

Charlton, M., G. T. Everson, S. L. Flamm, P. Kumar, C. Landis, R. S. Brown, Jr., M. W. Fried, N. A. Terrault, J. G. O’Leary, H. E. Vargas, A. Kuo, E. Schiff, M. S. Sulkowski, R. Gilroy, K. D. Watt, K. Brown, P. Kwo, S. Pungpapong, K. M. Korenblat, A. J. Muir, L. Teperman, R. J. Fontana, J. Denning, S. Arterburn, H. Dvory-Sobol, T. Brandt-Sarif, P. S. Pang, J. G. McHutchison, K. R. Reddy, and N. Afdhal. 2015. Ledipasvir and sofosbuvir plus ribavirin for treatment of HCV infection in patients with advanced liver disease. Gastroenterology 149(3):649-659.

Chhatwal, J., F. Kanwal, M. S. Roberts, and M. A. Dunn. 2015. Cost-effectiveness and budget impact of hepatitis V virus treatment with sofosbuvir and ledipasvir in the United States. Annals of Internal Medicine 162(6):397-406.

EASL (Eurpoean Association for the Study of the Liver). 2012. EASL clinical practice guidelines: Management of chronic hepatitis B virus infection. Journal of Hepatology 57(1): 167-185.

Edlin, B. R., B. J. Eckhardt, M. A. Shu, S. D. Holmberg, and T. Swan. 2015. Toward a more accurate estimate of the prevalence of hepatitis C in the United States. Hepatology 62(5):1353-1363.

Feld, J. J., K. V. Kowdley, E. Coakley, S. Sigal, D. R. Nelson, D. Crawford, O. Weiland, H. Aguilar, J. Xiong, and T. Pilot-Matias. 2014. Treatment of HCV with abt-450/r-ombitasvir and dasabuvir with ribavirin. New England Journal of Medicine 370(17):1594-1603.

HHS (Department of Health and Human Services). 2014. Action plan for the prevention, care, & treatment of viral hepatitis. Washington, DC: Department of Health and Human Services.

IHME (Institute for Health Metrics and Evaluation). 2016. Global burden of disease study 2013 (gbd 2013) data downloads—full results . http://ghdx.healthdata.org/global-burden-disease-study-2013-gbd-2013-data-downloads-full-results (accessed March 14, 2016).

Loria, P. 2016. This week in pharma: Questions for experts on Merck’s zepatier, Portola’s betrixaban . http://seekingalpha.com/article/3869636-week-pharma-questions-experts-mercks-zepatier-portolas-betrixaban (accessed March 14, 2016).

Martin, A. B., M. Hartman, J. Benson, and A. Catlin. 2015. National health spending in 2014: Faster growth driven by coverage expansion and prescription drug spending. Health Affairs (Millwood) 35(1):150-160.

Najafzadeh, M., K. Andersson, W. H. Shrank, A. A. Krumme, O. S. Matlin, T. Brennan, J. Avorn, and N. K. Choudhry. 2015. Cost-effectiveness of novel regimens for the treatment of hepatitis C virus. Annals of Internal Medicine 162(6):407-419.

Sanger-Katz, M. 2014. Boon for hepatitis C patients, disaster for prison budgets. The New York Times , August 7.

Ward, J. W., and J. H. Mermin. 2015. Simple, effective, but out of reach? Public health implications of HCV drugs. New England Journal of Medicine 373(27):2678-2680.

WHO (World Health Organization). 2015. Hepatitis B . http://www.who.int/mediacentre/factsheets/fs204/en (accessed January 15, 2016).

WHO. 2016 (unpublished). The case for investing in the elimination of hepatitis B and C as public health problems by 2030 .

Younossi, Z. M., H. Park, S. Saab, A. Ahmed, D. Dieterich, and S. C. Gordon. 2015. Cost-effectiveness of all-oral ledipasvir/sofosbuvir regimens in patients with chronic hepatitis C virus genotype 1 infection. Alimentary Pharmacology and Therapeutics 41(6):544-563.

Hepatitis B and C cause most cases of hepatitis in the United States and the world. The two diseases account for about a million deaths a year and 78 percent of world's hepatocellular carcinoma and more than half of all fatal cirrhosis. In 2013 viral hepatitis, of which hepatitis B virus (HBV) and hepatitis C virus (HCV) are the most common types, surpassed HIV and AIDS to become the seventh leading cause of death worldwide.

The world now has the tools to prevent hepatitis B and cure hepatitis C. Perfect vaccination could eradicate HBV, but it would take two generations at least. In the meantime, there is no cure for the millions of people already infected. Conversely, there is no vaccine for HCV, but new direct-acting antivirals can cure 95 percent of chronic infections, though these drugs are unlikely to reach all chronically-infected people anytime soon. This report, the first of two, examines the feasibility of hepatitis B and C elimination in the United States and identifies critical success factors. The phase two report will outline a strategy for meeting the elimination goals discussed in this report.

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• v.14(2); 2022 Feb

Viral Hepatitis as a Public Health Concern: A Narrative Review About the Current Scenario and the Way Forward

Ajeet s bhadoria.

1 Community and Family Medicine, All India Institute of Medical Sciences, Rishikesh, Rishikesh, IND

Anushikha Dhankhar

Giten khwairakpam.

2 Public Health Sciences, Treat Asia/amfAR, Bangkok, THA

Gagandeep Singh Grover

3 Public Health Sciences, Department of Health & Family Welfare, Chandigarh, IND

Vineet Kumar Pathak

4 Community and Family Medicine, All India Institute of Medical Sciences, Raipur, Raipur, IND

Pragya Pandey

Rohit gupta.

5 Gastroenterology and Hepatology, All India Institute of Medical Sciences, Rishikesh, Rishikesh, IND

Viral hepatitis is one of the emerging public health problems, which urgently needs special attention. The disease has a varied presentation at the time of diagnosis, and it can progress from an accidental finding to life-threatening conditions like liver cirrhosis. It belongs to the rare group of diseases that can cause chronic inflammation inside the body, and it can have a delayed presentation. It contributes substantially to the global burden on healthcare. In terms of mortality, the burden due to viral hepatitis is similar to that of HIV and tuberculosis. It is among the major global public health challenges along with other communicable diseases, such as HIV, malaria, and tuberculosis; the major difference is that there are very limited preventive models in place for viral hepatitis, especially in developing countries like India. With limited resources for diagnosis and treatment, varied levels of presentation, and a rapidly increasing burden, it can become the next silent pandemic. In the current review, the authors aimed to compile the available global strategies for combating hepatitis, protocols available for disease surveillance, and the salient points from the national program for hepatitis control in India [National Viral Hepatitis Control Program (NVHCP)], and propose some recommendations. Ensuring a health facility equipped with a rapid diagnostic kit for screening, proper lab for the confirmation, robust Health Management Information System (HMIS) portal for the data management, and organizing regular workshops for physicians and lab technicians are some of the recommendations that we put forward.

Introduction and background

Global burden: viral hepatitis as a public health concern

Viral hepatitis refers to a pathologic condition wherein an infection due to hepatitis viruses causes inflammation of the liver [ 1 ]. It contributes substantially to the global burden on healthcare, with 248 million people infected with hepatitis B and 71 million infected with hepatitis C worldwide [ 2 ]. It is among the major global public health challenges besides other communicable diseases, such as HIV, malaria, and tuberculosis [ 3 ]. According to the World Health Organization Progress report on HIV, viral hepatitis, and sexually transmitted infections, the condition was responsible for 1.4 million deaths in the year 2016 [ 4 ]. Among all deaths attributed to viral hepatitis, 96% were due to hepatitis B virus (HBV) (48%) and HCV (47%) alone [ 5 ]. In addition, viral hepatitis is also among the major causes of mortality in people living with HIV (PLHIV). Among PLHIV, the global estimate of the burden of HIV-HCV coinfection and HIV-HBV coinfection is 2.75 million and 2.6 million respectively [ 6 ]. The importance given to viral hepatitis prevention can be gleaned from the fact that it has been selected as Target 3 of the 2030 Agenda for Sustainable Development, which emphasizes an urgent need to prevent and control viral hepatitis [ 7 ].

Epidemiology of viral hepatitis (Indian scenario)

The burden of viral hepatitis in India is currently wide-ranged, mainly due to the paucity of data. According to the National Health Profile 2019 report, a total of 1,64,826 cases of viral hepatitis were detected in India in the year 2017, out of which 89,780 were men and 74,509 women, with a total of 537 deaths. Also, out of the 1,64,289 cases reported across India in the year 2017, the top 10 states with the highest burden of viral hepatitis were Bihar, Uttar Pradesh, Madhya Pradesh, Punjab, Delhi, Uttarakhand, Haryana, Maharashtra, and Rajasthan [ 8 ]. The proportion of hepatitis B surface antigen (HBsAg)-positive individuals in India ranges from 2 to 8%. It is also estimated that 15-25% of HBsAg carriers may later develop cirrhosis and cancer, consequently resulting in premature deaths. It has also been reported that around 40-50% of all hepatocellular carcinoma (HCC) cases are attributable to chronic HBV infection while HCV is responsible for 12-32% of HCC cases [ 9 ]. Also, 20-30% of all cirrhosis cases are due to chronic HBV infection while 12-20% are due to chronic HCV infection [ 10 ].

The present article aims to assess the current status of viral hepatitis national programs and strategies implemented for its prevention, control, and management. The authors aim to compile the available global strategies for hepatitis, protocols available for disease surveillance, and the salient points from the national program for hepatitis control in India [National Viral Hepatitis Control Program (NVHCP)] and offer some recommendations.

Global strategies: guidelines on hepatitis B and C testing, 2017

Global Health Sector Strategy (GHSS) on Viral Hepatitis, 2016-2021 is the first GHSS on viral hepatitis, a mission that is expected to contribute to the achievement of the 2030 Agenda for Sustainable Development. It covers the first six years of the post-2015 health agenda, 2016-2021, building on the Prevention and Control of Viral Hepatitis Infection: Framework for Global Action [ 2 ] and on two resolutions on viral hepatitis adopted by the World Health Assembly in 2010 and in 2014 [ 11 ]. The strategy addresses all five hepatitis viruses (hepatitis A, B, C, D, and E), with a particular focus on hepatitis B and C, owing to the relatively severe public health burden they represent. This strategy proposes eliminating viral hepatitis as a public health threat by 2030. The success of this strategy requires the diagnosis of 90% of infected individuals and treatment of 80% of the diagnosed cases with the aim of a 65% reduction in mortality. This strategy was last updated in 2016 and required changes regarding the time and course of treatment owing to three key developments, viz the evolution of direct-acting antiviral (DAA) regimens; a reduction in the need for conducting genotyping after the approval of DAA medicines that are pan-genotypic in nature; rapid rolling out of treatment in low- and middle-income countries due to substantial cost reduction of DAAs. These guidelines entail evidence-based recommendations for program managers and healthcare providers for treating persons with chronic HCV infection. Guidelines for the care and treatment were updated on the principle of "screening, care, and treatment", which were issued by the WHO Guidelines Review Committee in 2017 [ 12 ]. Low- and middle-income countries have been reporting the majority of cases of HBV and HCV infections. However, the burden is more pronounced among specific population groups, such as persons who inject drugs (PWID) and individuals from certain indigenous communities.

Protocol for the surveillance of the fraction of cirrhosis and hepatocellular carcinoma attributable to viral hepatitis in clinical centers of excellence, 2018

WHO recommends viral hepatitis surveillance that includes incidence of acute hepatitis and HBV and HCV prevalence, and mortality resulting from sequelae of liver disease, such as cirrhosis and HCC. Mortality reduction among HBV and HCV cases is used in the GHSS as one of the criteria for defining the goal of eliminating viral hepatitis as a public health threat by 2030 [ 10 ]. Therefore, laying down approaches to measure HBV- and HCV-related mortality are necessary. Initially, only deaths from acute infections were taken into account for measuring mortality; however, it ignored mortalities associated with chronic liver disease that resulted from hepatitis virus infection, such as cirrhosis and HCC.

Most countries do not have a systematic process to estimate national mortality rates from viral hepatitis, thereby needing to convert ad hoc approaches used in various research studies into routine surveillance systems. For this, deaths resulting from chronic liver disease (including cirrhosis and HCC) and the fraction of disease conditions that can be attributed to various hepatitis viruses can be used to estimate mortality. This protocol describes approaches that can be utilized in sentinel centers (e.g., hepatology or gastroenterology units) to estimate the proportion of individuals with cirrhosis and HCC due to HBV and HCV. This data is crucial to estimate the prevalence of cirrhosis and HCC, individuals in the advanced stage of liver disease, and mortality as a result of cirrhosis or HCC. The cases of cirrhosis and HCC can be followed up to understand the trends in disease development [ 13 ].

Hepatitis control through multi-disease testing

Although HIV-associated deaths have been controlled by antiretroviral therapy (ART), morbidity and mortality associated with coinfections like TB, HBV, and HCV pose a threat to investments in treatment. In 2016, approximately 2.75 million HIV patients also suffered from HCV coinfection [ 14 ]. Late detection of these coinfections results in infection progressing to an advanced stage by the time the patient reports to a healthcare facility, leading to costly care and management at the patient level. These coinfections also have a high potential for HIV transmission, its progression, and associated mortality. This necessitates the need to scale up screening for HIV and other coinfections in high-risk populations [ 15 , 16 ]. Multi-disease diagnostic platforms can help identify the presence of multiple infections and variations in the pathogen along with associated antimicrobial resistance. This will help streamline and simplify diagnosis and further management of multiple infectious diseases, thereby reducing cost, improving access for patients, and eventually controlling these outbreaks [ 17 ].

Elimination of hepatitis C virus infection in children, 2018

Approximately 6-11% of children acquire HCV from their infected mothers [ 18 ]. Out of these, only 20% show clearance within two years from birth, while the rest do not and develop chronic HCV infection later in life. As a result, these children are more likely to develop liver disease, which also tends to get severe with age. Adding to the problem is the limited preventive strategies and lack of evidence of their safety. DAAs have revolutionized HCV treatment across the world; however, evidence on their safety during pregnancy is scarce [ 19 ].

Standard operating procedures for enhanced reporting of cases of acute hepatitis, 2018

As per WHO, the surveillance of viral hepatitis must cover three key indicators of the disease burden: incidence (new infections of acute hepatitis), prevalence (chronic hepatitis cases), and mortality as a result of sequelae of infection including HCC and liver cirrhosis. To achieve a reduction in the incidence of HBV and HCV, countries need to adopt methods that identify associated risk factors. Although a major proportion of cases (50-70% for HBV and >80% for HCV) are asymptomatic, information on diagnosed symptomatic new infections can prove truly helpful and is the only way to study the change in disease trends among new infections in the community [ 20 ].

Progress on viral hepatitis, 2019: global targets, service coverage, and current status

Thanks to the ongoing hepatitis immunization and prevention programs, the incidence of hepatitis infection, especially hepatitis B, has declined. However, the reduction in mortality rates has been negligible, and this requires intervention for improving testing and treatment access. According to the WHO’s Progress Report [ 4 ] on HIV, Viral Hepatitis and Sexually Transmitted Diseases, 2019, the targets for 2020 and 2030 for viral hepatitis included a 30% reduction by 2020 and a 90% reduction by 2030 in the number of new chronic viral hepatitis B and C infections. Data suggest that in the year 2017, 1.1 million new cases of chronic hepatitis B were diagnosed; however, for chronic hepatitis C, only baseline data for the year 2015 is available, which reported 1.75 million newly diagnosed cases [ 21 ]. For reducing mortality, a target of 10% reduction by 2020 and 65% by 2030 was set for hepatitis B and C. However, only baseline data from the year 2016 is available, showing a total of 1.4 million deaths due to all types of viral hepatitis infections [ 22 ].

In order to achieve the 2030 targets for service coverage, the expedition of testing and treatment is necessary. Despite a strong immunization coverage program, the proportion of first doses given at birth is low [ 8 ]. Services to prevent mother-to-child transmission of HBV were set to have 50% coverage by 2020 and 90% coverage by 2030. As of 2017, there has been 43% global coverage of the services through a timely hepatitis B vaccination at birth [ 23 ]. About 97% of the blood donations were screened for quality assurance (as per baseline data of 2015) against a target of achieving 95% screening by 2020 and 100% by 2030 [ 2 ]. In the year 2017, 3.9% injection reuse was reported against a target of 50% injections to be administered following safety-engineering devices by 2020 and 90% by 2030. Harm-reduction services have also been observed to be in urgent need of action with only 33 needle sets provided per injection drug user in 2017 against the target of 200 sterile needle sets per injection drug user by 2020 and 300 by 2030 [ 24 ]. Diagnostic and treatment services also need to be made more equitable and accessible to achieve a target of diagnosing 30% of chronic viral hepatitis B and C cases by 2020 and 90% by 2030. However, only 10% (27 million) [ 25 ] of people with chronic hepatitis B and 19% (13.1 million) with chronic hepatitis C knew their status as per the 2016 baseline data. Out of these, only 4.5 million (17%) eligible and diagnosed chronic hepatitis B cases had been treated by the year 2016 and only five million diagnosed chronic hepatitis C cases by the year 2017 against a global target of 80% treatment coverage by 2030 [ 21 ].

Consolidated strategic information guidelines for viral hepatitis, 2019: planning and tracking progress towards elimination, 2019

Aiming to eliminate viral hepatitis as a public health threat by 2030, the first GHSS on viral hepatitis was endorsed by the World Health Assembly in the year 2016. The GHSS includes the implementation of five core interventions at an acceptable level of service coverage. These five core interventions include immunization, preventing vertical transmission of HBV, safe injection and blood transfusion, harm reduction for high-risk populations (e.g., those using injectable drugs), and testing and treatment. For the purpose of monitoring and evaluation, surveillance and documentation of cases, prevention, testing, and treatment of viral hepatitis have been implemented. The strategy also emphasizes the importance of implementing collaborative efforts in viral hepatitis programs with other different health programs, such as communicable disease control, HIV, TB, cancer care, immunization, and primary care to assist data collection and analysis without the need to set up separate systems [ 26 ].

Current status of National Viral Hepatitis Control Program (NVHCP): widening the scope

In India, HBsAg positivity in the general population ranges from 1.1 to 12.2%, with an average prevalence of 3-4%. Anti-HCV antibody prevalence in the general population is estimated to be between 0.09-15% [ 27 ]. Population-based syndromic and health facility-based surveillance of viral hepatitis is mandated under the Integrated Disease Surveillance Programme (IDSP). In India, approximately 40 million people are chronically infected with hepatitis B and 6-12 million people with hepatitis C. On the occasion of World Hepatitis Day on 28th July 2018, the Ministry of Health and Family Welfare, Government of India launched the NVHCP [ 28 ]. The program covers all types of viral hepatitis infections (from A to E) and comprehensively focuses on all aspects, such as prevention of infection, early identification and treatment, and mapping of treatment outcomes. The program was launched along with the release of its operational guidelines, national laboratory guidelines for viral hepatitis testing, and national guidelines for the diagnosis and management of viral hepatitis.

On 24th February 2019, an advocacy event, "India’s Response to Viral Hepatitis", was held and Technical Guidelines for Diagnosis and Management of Hepatitis B and National Action Plan-Combating Viral Hepatitis in India were released, and the NVHCP website was launched. On World Hepatitis Day, 2019, the inauguration of the model treatment program was conducted at Sion Hospital, Mumbai, and the user manual of the NVHCP-MIS for hepatitis C and a national helpline number for viral hepatitis (1800-11-6666) were launched. Additionally, social media campaigns on prevention, identification of high-risk groups, the risk among pregnant women, as well as treatment-oriented campaigns about free drugs and diagnostics for hepatitis B and C, and laboratory testing and management of viral hepatitis were also created and run.

The program adopted an integrated approach and collaborated with other programs and schemes to provide a promotive, preventive, and curative package of services for individuals suffering from viral hepatitis. Under the ‘Training of Trainers’ initiative of the program, 800 experts were trained on diagnosis and management of viral hepatitis and NVHCP-MIS, while training on viral hepatitis, modes of transmission, and prevention were conducted for community members. Regular review and coordination meetings were also held. In addition, two national-level workshops were held for nodal officers to sensitize them about the services provided under the program. For state principal secretaries, mission directors, and state nodal officers for monitoring the program, video conferences were held twice.

The program has also seen major changes with respect to the existing infrastructure. Currently, model treatment centers have been established in all states and six union territories (UTs). This includes the establishment of 301 treatment centers in 285 districts for service delivery under the program. Nine states have made treatment sites functional in all the districts: Bihar, Haryana, Jharkhand, Kerala, Maharashtra, Mizoram, Nagaland, Punjab, and Rajasthan. Approximately 6.5 lakh serological tests have been done as of now for the diagnosis of viral hepatitis C and 16 lakh tests for hepatitis B, and more than 38,000 patients have been put on treatment for hepatitis C. The infection safety committee has been reconstituted. For enhancing skills and capacity building, the Extension for Community Healthcare Outcomes (ECHO) platform is being utilized for online clinical case discussion and conducting training for healthcare workers.

The main activities of the program involve prevention, diagnosis and treatment, monitoring and evaluation, surveillance and research, and review meetings. The NVHCP is coordinated by the center and state bodies. The National Viral Hepatitis Management Unit (NVHMU) is the center-level body and it controls and evaluates the implementation of programs across the country. The State Viral Hepatitis Management Unit (SVHMU) manages the program at the state level through a nodal officer of the State Health Society. At the district level, the program officer of the District Viral Hepatitis Management Unit (DVHMU) supervises program implementation and manages various activities such as supply chain management, outreach services, and logistics and training. Regarding the allocation of funds, the NVHMU at the center level is responsible for developing a program implementation plan (PIP) for states for achieving annual targets, and supervising, monitoring, and evaluating the overall program. The SVHMU assigns a nodal officer for program implementation at the state and district levels and develops PIP to be discussed and improvised after the approval from NVHMU. The DVHMU deals with ensuring the functionality of labs and treatment centers, identifying potential service delivery sites, training of staff, developing referral linkages, ensuring multi-program linkage, IEC material distribution, and data collection and reporting at the district level.

With the focus on the chronicity of the disease, the first cornerstone key component of the program was prevention through awareness generation, immunization against hepatitis B, and adhering to safe blood and injection practice. Early diagnosis through screening of pregnant women, and community involvement can boost adherence if treatment is placed as a second key component. Under the monitoring and evaluation component, effective linkages to the surveillance system would be established and operational research would be undertaken through the Department of Health Research (DHR) through an online web-based system. The last component as training and capacity building would be a continuous process and will be supported by National Centre for Disease Control (NCDC), the Institute of Liver and Biliary Sciences (ILBS), and state tertiary care institutes and coordinated by NVHCP. It would include the traditional cascade model of training through master trainers and various platforms available for enabling electronic, e-learning, and e-courses.

With the program being in its fourth year, a few challenges have been faced in successfully implementing it. The first concern is infrastructure and material management. Proper planning for the estimation of drugs and rapid diagnostic kits is a matter of huge concern for timely procurement and dissemination of materials. Also, the mobilization of human resources for effective service delivery in each district is a big challenge. Optimum procurement of quality testing kits, increasing viral load testing, reporting on the MIS platform, regular monitoring, and review of the program along with supportive supervision at all levels are some focus areas needing an immediate call to action.

Recommendations

Since the program is using preexisting healthcare infrastructure, it should be ensured that the healthcare facility that is designated as a treatment center is provided with rapid diagnostic kits for screening, machinery required for lab investigation, drugs, and a well-developed Health Management Information System (HMIS) portal. Program management units should disburse screening kits in a planned way for maximum utilization; this includes the distribution of kits in a tiered manner by following a top-to-bottom approach. Free-of-cost screening kits should be made available for screening key and bridge populations, as well as antenatal and preoperative screening. The willingness among the population and yield of screening for hepatitis should be studied [ 29 ]. There should be a well-established system for notification, confirmatory and auxiliary tests as well as treatment of rapid diagnostic test-positive patients. A decentralized approach could be adopted for better outcomes [ 30 ].

Many treatment centers (district hospitals) are not equipped with facilities for basic laboratory investigations to manage viral hepatitis, such as coagulation profile (PT/INR); in some centers, there is no HMIS portal, while in some other centers, even though screening kits and drugs are available, physicians are not aware of the program through which the logistics have been supplied. A well-developed HMIS portal may resolve these issues. Organizations like the Clinton Health Access Initiative (CHAI) and ECHO have shown promising results in the state of Punjab, and other states could also take assistance from these organizations for data management and capacity building [ 31 , 32 ]. The program has the provision for appointing human resources in the form of a medical officer, laboratory technician, data entry operator, and peer supporter. However, at some of the management units and treatment centers, the required staff has not been appointed yet; instead, there is a provision for incentivizing the preexisting healthcare workers. Considering the burden of patients, the feasibility of incentivization is questionable [ 33 ]. Moreover, many of these healthcare workers are appointed by the state and report to the chief medical officer at the district level rather than the district nodal officer for NVHCP, which sets two parallel systems in place; commissioning human resources exclusive to run the program could resolve this issue. Strengthening peer support can enable patient engagement with healthcare services, particularly for marginalized populations [ 34 ]. Under NVHCP, training workshops for physicians and lab technicians are routinely organized. The scope of such workshops needs to be broadened to include program managers, data entry operators, and peer supporters in order to have well-oriented and accountable staff at every level. Capacity-building should be synchronized with the development of infrastructure and human resources. Judicious nomination of specialty resources should be done for training, with a focus on training internists from centers where infrastructure and human resources have been provided.

There is a necessity for regular monitoring and conducting evaluation meetings and visits, as this can help understand the strengths and gaps in the implementation of the program at the grassroots level. Finally, based on the ground reports, state steering committees should remodel the operational guidelines for each state. It is also recommended to publish these reports to disseminate the best practices and strategies to overcome challenges.

Conclusions

The burden of viral hepatitis is increasing globally as well as in India. Being among the most populous countries, India contributes significantly to the disease burden. Despite having prevalence rates similar to HIV, tuberculosis, and malaria, political commitment and efforts made in the direction of prevention and control of viral hepatitis need more attention. Although the current scenario with respect to NVHCP has improved over the past few years, infrastructural, resource-related, and service-provision scenarios are still in a budding stage and need an urgent call to action owing to the growing burden of the disease at a faster rate than before. The program has a long way to go; however, with better initiatives at each level of the continuum of hepatitis control and prevention, appropriate action and care can contribute to improving the current trends and can accelerate the progress towards achieving the Sustainable Development Goal 3.3 sooner than expected.

The content published in Cureus is the result of clinical experience and/or research by independent individuals or organizations. Cureus is not responsible for the scientific accuracy or reliability of data or conclusions published herein. All content published within Cureus is intended only for educational, research and reference purposes. Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus.

The authors have declared that no competing interests exist.

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Hepatitis B Essay

Hepatitis B

Page 2 Hepatitis B is a potentially life threatening liver infection caused by the virus HBV. A Hepatitis B infection could potentially become a chronic disease for some people because they run the risk of developing liver failure, cirrhosis of the liver or liver cancer if precautions are not taken. Cirrhosis causes permanent scarring to the liver. Some adults that have become infected with Hepatitis B do fully recover even if their symptoms are relentless. Symptoms can be mild to

Running head: EPIDEMIOLOGY PAPER - HEPATITIS B 1 Epidemiology Paper - Hepatitis B Concepts in Community and Public Health NRS-427V-0102 EPIDEMIOLOGY PAPER - HEPATITIS B Epidemiology Paper - Hepatitis B 2 ―Communicable disease‖ means an illness caused by an infectious agent or its toxins that occurs through the direct or indirect transmission of the infectious agent or its products from an infected individual or via an animal, vector or the inanimate environment to a susceptible animal

Epidemiology Hepatitis B Infection

Epidemiology Hepatitis B Dheer Chhabria MYP2A EPIDEMIOLOGY HEPATITIS B 1 The Causative Agent of Hepatitis B Infection The causative agent of the hepatitis B infection, known as serum hepatitis, is a Hepadna virus that attacks the liver causing inflammation of the liver . If this disease is left untreated it can result in liver cirrhosis , liver cancer, liver failure and death. The liver cancer caused by hepatitis B the virus is called Hepato Cellular Carcinoma which is the third most common cause

Epidemiology Hepatitis B

Epidemiology Hepatitis B affects 1 in 3 people worldwide (Hepatitis B Foundation [HBF], 2014). A vaccine has been available for over 30 years, yet it is the ninth leading cause of death worldwide (HBF, 2014). The epidemiology of hepatitis B, the role of the community health nurse along with the knowledge about what is being done to combat and reduce the impact of the virus gives a comprehensive look at hepatitis B. Hepatitis B virus (HBV) is a DNA virus, and belongs to the Hepadnaviridae family

Hepatitis B What is hepatitis B? Hepatitis means the inflammation of the liver. Hepatitis B, “formerly called serum hepatitis (Richard Adler)”, is caused by a serious liver infection with the hepatitis B virus (HBV) and the infection has two phases: acute and chronic (eMedicineHealth). Acute hepatitis B is short-term and occurs after being exposed to the virus and only few develop fulminant hepatitis which is very severe and life threatening. Chronic hepatitis can lead to “liver failure, liver

Hepatitis B Case Studies

said to be affected with hep-B in the United States than children. Since 1990 the routine for immunization against the disease has led to a decline in children for the past decades. African Americans are infected with the disease than either Hispanics or Caucasians, Alaskan Eskimos and Pacific Islanders however have a higher carrier status rate than other racial groups. Compared other racial groups Asian Americans are at increased risk of severe liver damage from hepatitis B. More males than females

Hepatitis B Research Paper

to offer, but what if they could do more? Bananas are also one of the best candidates to deliver oral vaccines for the hepatitis B Virus (HBV). Hepatitis B is caused by the hepatitis B virus (HBV) is a viral infection affecting the liver that can lead to serious illness or death, usually found in blood. There are approximately three hundred and fifty million carriers of hepatitis B in the world, an estimated amount of seventy five million to one hundred million of those infected with the virus dying

Mmwr Hepatitis B

MMWR Paper on Hepatitis B Microbiology 212-A April 27, 2012 Hepatitis B virus (HBV) is a DNA virus that affects the liver and belongs to the Hepadnaviridae group (Takkenberg, Weegink, Zaaijer, & Reesink, 2010). According to an article in Vox Sanguines, an international journal of transfusion medicine, (Takkenberg, Weegink, Zaaijer, & Reesink, 2010) “about 400 million people worldwide are chronically infected with HBV, and 2 billion people have serological evidence of past or present

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Hepatitis B Vaccine Hepatitis B is the most common liver infection in the world and is caused by the hepatitis b virus. The hepatitis b virus enters the body and travels to the liver via the bloodstream. In the liver the virus attacks the healthy liver cells and then multiplies. The cells create copies of them selves and the multiplying of the virus cells then triggers a response from the bodies’ immune system. Most people at this stage of the virus are unaware the have the virus as there are no

Hepatitis B Case

In Hepatitis B, it is the biggest part of your body your liver, it helps your body digest food and stores energy and also remove poison. What is Hepatitis B? A swerve from viral hepatitis transmitted in infected in the blood causing a fever and debility and jaundice. In Hepatitis B, you can also contact people by blood, semen or body fluids. How do you know if you have Hepatitis B? by yellow of skin of the eye, dark color urine and you will have pale movements. The worst part of having Hepatitis

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Essay on Viral Hepatitis

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In this essay we will discuss about Viral Hepatitis. After reading this essay you will learn about: 1. Introduction to Hepatitis 2. Pathology of Hepatitis 3. Pathogenesis for Hepatitis 4. Hepatitis Vaccine 5. Classification of Hepatitis.

• Essay on the Classification of Hepatitis

Essay # Introduction to Hepatitis:

Viral hepatitis is a systemic disease with primary inflammation in the liver. Most of the viral hepatitis resemble each other in clinical symptoms; whereas Hepatitis B viral infection is mostly severe and fatal. Many cases of hepatocellular carcinoma are due to Hepatitis B and C viruses.

Essay # Pathology of Hepatitis:

The lesions in liver produced by all types of hepatitis viruses are similar and consist of infiltration of mononuclear cells (mainly lymphocytes), necrosis of hepatic cells, hyperplasia of Kupffer cells and variable degree of cholestasis. Parenchymal cell damage is due to hepatic cell degeneration and necrosis, ballooning of single cells and acidophilic degeneration of hepatocytes as they die.

In healthy carrier and chronic hepatitis due to Hepatitis B virus (HBV), large hepatocytes with a ground glass appearance of the cytoplasm may be seen; these cells contain Hepatitis B surface Antigen (HB s Ag). In chronic hepatitis, there is piece meal necrosis at first and later on fibrosis occurs which ultimately leads to cirrhosis, hepatocellular carcinoma.

Essay # Pathogenesis for Hepatitis:

Though Hepatitis viruses differ antigenically, their clinical features are almost similar. These viruses cause acute inflammation of the liver with a clinical picture characterised by fever, anorexia and malaise followed by nausea, vomiting and liver tenderness (pre-icteric phase). This phase may last for a few days and sometimes it may continue longer (3 weeks or more).

As this phase subsides, the icteric phase appears with jaundice with dark urine, pale stools, obstructive jaundice with a slow recovery period of 4-6 weeks and longer severe cases. Symptomless or minor infection is also common in HAV and HEV types.

Essay # Hepatitis Vaccine:

Potato vaccine offered hope against Hepatitis A virus vaccine grown in genetically engi­neered potatoes—seemed to protect more people who ate them, reported by Times of India in February 2005.

About 60% of the volunteers who ate these potatoes showed an immune response that should protect against infection with hepatitis B virus that is shown to stimulate the immune system response.

Antibodies raised in most of 60% volunteers who ate more than three pieces of the genetically engineered potatoes and more than those who ate two pieces.

Hepatitis B virus vaccine shot should be kept refrigerated and expensive—meaning that it cannot be used in many poor countries. People prefer edible vaccine than to get a shot.

Scientists are working to grow the vaccine in banana, tomato or tobacco.

In 1996, 115 million people were infected with HBV even though vaccine isolated from yeast became available in 1986.

Global mortality due to HBV was to be one million cases per year. Hepatitis B vaccine booster was not required as published in Lancet, 2005—reported in Times of India (Oct. 2005) because of immunizing effect of Hepatitis B vaccine lasts for ten years. Infants and adolescent immune system recalls the response to Hepatitis B virus for more than 10 years after immunization.

Essay # Classification of Hepatitis:

There are six major types of primary hepatotrophic, acute hepatitis viruses. Besides, other viruses are also responsible for acute viral hepatitis.

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• Essay on Hepatitis A Virus (HAV)
• Essay on Hepatitis B Virus (HBV)

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Hepatitis D infection: from initial discovery to current investigational therapies

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Ben L Da, Theo Heller, Christopher Koh, Hepatitis D infection: from initial discovery to current investigational therapies, Gastroenterology Report , Volume 7, Issue 4, August 2019, Pages 231–245, https://doi.org/10.1093/gastro/goz023

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Hepatitis D is the most severe form of viral hepatitis associated with a more rapid progression to cirrhosis and an increased risk of hepatocellular carcinoma and mortality compared with hepatitis B mono-infection. Although once thought of as a disappearing disease, hepatitis D is now becoming recognized as a serious worldwide issue due to improvement in diagnostic testing and immigration from endemic countries. Despite these concerns, there is currently only one accepted medical therapy (pegylated-interferon-α) for the treatment of hepatitis D with less than desirable efficacy and significant side effects. Due to these reasons, many patients never undergo treatment. However, increasing knowledge about the virus and its life cycle has led to the clinical development of multiple promising new therapies that hope to alter the natural history of this disease and improve patient outcome. In this article, we will review the literature from discovery to the current investigational therapies.

Hepatitis D is a rare form of viral hepatitis that was first described in 1977 by Rizzetto et al . through immunofluorescence detection of the delta antigen and anti-delta antibody in the serum and liver tissues of hepatitis B surface antigen (HBsAg) carriers [ 1 ]. While it has been estimated to affect 15–20 million people worldwide, more recent data suggest that the global disease burden may be closer to 62–72 million [ 2 ]. Hepatitis D virus (HDV) is an incomplete RNA virus that requires the assistance of the hepatitis B virus (HBV), specifically the HBsAg, to be infectious in humans [ 3 ]. Once chronicity is established, HDV has been described as the most severe form of viral hepatitis, with progression to cirrhosis in 10%–15% of patients within 2 years and in 70%–80% of patients within 5–10 years [ 4 , 5 ]. Despite this, a lack of adequate treatment options currently exists for HDV. Current international guidelines suggest the use of pegylated-interferon-α (peg-INF-α), although sustained virological response (SVR) rates with this treatment are reported to be only 20%–30% [ 6–8 ]. In addition, even after SVR is achieved, late relapse remains an issue [ 9 ]. Recent advances in our understanding of the HDV viral cycle have led to the development of several promising investigative therapies that are under investigation.

In this piece, we review the virology, epidemiology, diagnosis, clinical presentation, natural history, outcomes and the available and investigative treatments pertaining to this disease.

Viral structure and life cycle

HDV is a small, spherical RNA virus measuring ∼36 nm in diameter with an inner nucleocapsid that consists of a short (∼1.7-kb) single-stranded, circular RNA and approximately 200 molecules of hepatitis D antigen (HDAg) [ 10 , 11 ]. This viral genome is the smallest among known mammalian viruses and shares structural similarity to viroid RNAs [ 12–14 ]. It encodes for a single protein, the HDAg, which exists in two forms: the small HDAg (S-HDAg) and large HDAg (L-HDAg). Structurally, the two forms are identical except that the L-HDAg has an additional 19 amino acid sequence at the C-terminus [ 15 ]. The outer coat of the HDV virion consists of components taken from HBV, thus mandating a co-infective process with HBV, which includes the small, medium and large HBsAg [ 3 ]. The isoforms of HBsAg are embedded in a lipid envelope surrounding the HDV genome and HDV antigen isoforms. The large HBsAg then undergoes a process called myristoylation at the N-terminus to prepare for cell entry [ 16–18 ]. The life cycle of HDV is depicted in Figure 1 . First, the HDV virion binds to the human hepatocyte through an interaction between the myristoylated N-terminus of the pre-S1 domain of the large HBsAg and the host receptor, which has been identified as the multiple transmembrane receptor sodium taurocholate cotransporting polypeptide (NTCP) located on the basolateral membrane of hepatocytes [ 19 , 20 ]. After entry, the HDV genome is translocated to the nucleus via the HDAg [ 21 ]. Upon arriving in the nucleus, HDV commandeers host RNA polymerase II, a DNA-directed RNA polymerase, for transcription of HDV RNA [ 22 ]. Replication of the HDV occurs through a rolling-circle mechanism [ 12 , 23 ]. The initial step is synthesis of multimeric linear transcripts from the circular genomic template. Afterwards, these multimeric linear transcripts are cleaved into monomers by autocatalytic self-cleaving sequences called ribozymes. Subsequently, monomer RNAs are ligated by the ribozyme into an antigenomic, monomeric, circular RNA that serves as a template for another round of rolling-circle replication. The finished product is a circular genomic HDV RNA [ 13 ].

Hepatitis D virus viral life cycle and sites of drug target. 1. Hepatitis D virus (HDV) virion attaches to the hepatocyte via interaction between hepatitis B surface antigen proteins and the sodium taurocholate cotransporting polypeptide (NTCP), a multiple transmembrane transporter. 2. HDV ribonucleoprotein (RNP) is translocated to nucleus mediated by the hepatitis D antigen (HDAg). 3. HDV genome replication occurs via a ‘rolling-circle’ mechanism. 4. HDV antigenome is transported out of the nucleus to the endoplasmic reticulum (ER). 5. HDV antigenome is translated in the ER into small HDAg (S-HDAg) and large HDAg (L-HDAg). 6. L-HDAg undergoes prenylation prior to assembly. 7. S-HDAg is transported back to the nucleus where it supports HDV replication. 8. New HDAg molecules are associated with new transcripts of genomic RNA to form new RNPs that are exported to the cytoplasm. 9. New HDV RNP associates with hepatitis B virus (HBV) envelop proteins and assembled into HDV virions. 10. Completed HDV virions are released from the hepatocyte via the trans-Golgi network.

Three different RNAs are generated during the replication process: the HDV genome, the antigenome that is its exact complement and a third smaller antigenome that contains the open reading frame (ORF) that codes for the HDAg [ 22 ]. During replication, the HDV genome and antigenome collapses into a characteristic unbranched rod-like structure [ 24 ]. Both forms of HDAg are translated in the endoplasmic reticulum from the ORF located on the antigenomic HDV RNA strand [ 25 ]. The S-HDAg plays a significant role in replication, since it is required for RNA synthesis, while the L-HDAg inhibits RNA synthesis and is required for packaging. Cellular adenosine deaminase acting on RNA (ADAR) editing of the amber codon on the viral antigenome RNA enables the HDV to switch from replication to packaging [ 24 ].

The HDV RNA and HDAg proteins interact to form a ribonucleoprotein (RNP) particle at a molar ratio of 200 [ 12 , 26 ]. The modification of post-translation HDAg proteins is essential for this process but is also crucial for HDV replication and HDV-virion assembly [ 27 , 28 ]. One of these post-translational modification processes is called farnesylation, which is crucial for HDV-virion assembly and serves as a target for drug action. At the C-terminal of the L-HDAg is a 19-amino acid polypeptide that includes the C-terminal CXXX-box motif (where C = cysteine and X = any amino acid), which is the substrate for prenyltransferases to add a prenyl lipid group [ 15 , 29 ]. Farnesyl is one of the prenyl groups that can be added via the enzyme farnesyltransferase in a process specifically called farnesylation. Farnesylation anchors the RNP to the endoplasmic reticulum membrane where HBV envelop proteins are made and then makes the RNP more lipophilic and more amenable to interactions with HBsAg. This C-terminal 19-amino acid residue region, which is not well conserved between different HDV genotypes, plays a key role in the varied assembly efficiencies between genotypes, which likely has pathologic implications [ 30–32 ]. Interestingly, HBV envelope proteins are made in excess so, even when HBV is suppressed, additional HDV virions can still be assembled [ 33 ].

Finally, once the RNP interacts with the envelop protein of HBV and the HDV is assembled, the HDV virion is now ready for release. The HDV virion is released via the trans-Golgi network, where it can go on to infect other hepatocytes. However, the exact mechanism of HDV-virion release remains unknown [ 15 ].

Viral genotypes

To date, eight distinct HDV genotypes have been recognized, with two to four subtypes per genotype characterized by >90% similarity over the entire genome sequence [ 2 , 34 , 35 ]. The geographical distributions of the HDV genotypes have changed over time, most probably due to human migration patterns. Currently, genotype 1 is the most prevalent worldwide and the predominant genotype in Europe and North America [ 36 ]. Genotype 2 was previously confined to Asia but has now emerged in Middle Eastern countries including Iran [ 37 ] and Egypt [ 38 ]. Genotype 3 is mainly found in the Amazon Basin in South America and is the most different of all the genotypes exhibiting ∼40% divergence at the nucleic acid level [ 39 ]. Genotype 4 is predominately found in Taiwan, China and Japan [ 35 ]. Meanwhile, genotypes 5, 6, 7 and 8 have traditionally been found only in Africa, but recent reports describe the migration genotypes 5, 6 and 7 to various parts of Europe [ 40–42 ]. Notably, central Africa is thought to be main site of HDV diversification, with the presence of genotypes 1, 5, 6, 7 and 8 [ 35 ].

It is well known that specific HDV genotypes influence clinical outcomes. HDV genotype 3 appears to be the most pathogenic of all the HDV genotypes [ 43 , 44 ]. HDV genotype 1 patients have lower rates of remission, more aggressive disease and worse outcomes than HDV genotype 2 patients [ 45 , 46 ]. For example, in a study from Taiwan, Su et al . reported significantly lower rates of remission in HDV genotype 1 compared to HDV genotype 2 (15.2% vs 40.2%, P  =   0.007) and more adverse outcomes (cirrhosis, hepatocellular carcinoma [HCC] or mortality) (52.2% vs 25.0%, P  =   0.005) [ 45 ]. This is likely due to HDV genotype 1 being a more efficient genotype in terms of virion assembly and RNA editing than genotype 2, resulting in the secretion of more viral particles [ 31 , 32 ].

Epidemiology and risk factors

The seroprevalence of HDV among HBsAg-positive carriers has substantial variations worldwide. These are depicted in Table 1 . Interestingly, more recent data have shown that 8% of the general Mongolian population is estimated to be positive for HDV [ 2 ]. Notably, in the USA, the prevalence of HDV among HBV carriers has been reported to range from 2% to 50%, depending on the patient population [ 63–66 ]. A large study of the US Veteran’s Affairs medical system more recently reported an HDV seroprevalence of 3.4% among patients with chronic HBV who are tested for HDV [ 78 ]. A study using the National Health and Nutrition Examination Survey reported a HDV seroprevalence of 42% among HBV carriers [ 65 ]. Finally, the highest estimation of HDV seroprevalence came from a study of HBV-positive intravenous drug users (IVDU), which showed that the seroprevalence of HDV increased from 29% in 1988–1989 to 50% in 2005–2006 [ 66 ]. However, a general lack of HDV RNA validation in these studies prevents estimation of true HDV prevalence.

Epidemiology of hepatitis D

Despite the various HDV epidemiological reports, there continues to be insufficient data on the true global prevalence of HDV [ 2 ]. This is attributable to several factors. First, reported rates are likely to be underestimations, stemming from incomplete population testing because of a lack of clinician awareness resulting in a lack of diagnosis along with a lack of availability of HDV clinical tests. In a nationwide study in the USA of 25   603 HBV patients, only 8.5% of patients were ever tested for HDV [ 78 ]. Manesis et al . reported that only a third of Greek patients with chronic hepatitis B (CHB) were tested for HDV [ 55 ]. El Bouzidi et al . similarly reported that only 40% of British chronic HBV patients were tested for anti-HDV in patients with positive HBsAg [ 40 ]. Special focus also needs to be made for HDV testing among patients with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) due to a high rate of co-infection because of shared risk factors such as transfusions, tattooing, IVDU and high-risk sexual practices [ 79 ]. For example, reported co-infection rates with HCV have ranged from 26%–73% [ 42 , 48 , 53 , 68 ] and HIV of 12.7% [ 42 ].

Second, studies from the same country have reported discrepant numbers that may be due to significant geographical variations even within the same country. For example, a meta-analysis from Turkey described that the HDV seroprevalence of west Turkey was 4.8%, while the seroprevalence of HDV in southeast Turkey was 46.3% [ 80 ]. In addition, most of the epidemiologic studies on the seroprevalence of HDV among chronic HBV patients did not require HDV polymerase chain reaction (PCR) confirmation as an inclusion factor, further preventing the estimation of the true prevalence of HDV. Finally, the timing of the publication is also important because the seroprevalence of HDV declined drastically after the late 1980s due to the implementation of HBV vaccine programs around the world [ 81–83 ].

Despite an earlier notion that HDV was a disappearing disease in many parts of the world, this has proven to be no longer the case. In fact, more recent data have shown that the prevalence of HDV has remained stable or has increased in many endemic and non-endemic countries due to an increase in associated risk factors such as immigration, IVDU, men-who-have-sex-with men (MSM) and intra-familial spread [ 41 , 67 , 71 , 79 , 84 , 85 ]. For example, a collection of studies from Italy reported a decline in the prevalence of HDV among HBsAg-positive patients from 23% in 1987 to 14% in 1992 to 8.3% in 1997, which was attributed to HBV-vaccination programs [ 67 , 86 , 87 ]. However, more recent data have suggested that the prevalence of HDV in Italy has either remained stable at 8.1% [ 85 ] or has rebounded to 11.3% [ 84 ]. Lin et al . showed that the prevalence of HDV increased from 38.5% to 89.8% among HIV-infected IVDU patients with HBV from 2001 through 2012 [ 71 ]. Furthermore, outbreaks of HDV have been especially rampant among areas of with low social-economic levels [ 79 , 80 ]. Due to immigration from endemic countries, multiple studies have reported an increase in the prevalence of HDV in countries in which HDV was previously uncommon [ 48 , 49 , 53–55 ]. In a study by Coghill et al . from Australia, those born in Africa were shown to have a higher risk ratio (RR) for HDV infection (RR, 1.55; 95% confidence interval [95% CI], 1.14–2.09) [ 48 ]. Cross et al . reported in a study from England that over half of their HDV patients were from regions of the world where HDV is endemic including Southern or Eastern Europe (28.1%), Africa (26.8%) and the Middle East (7.3%) [ 53 ]. Similarly, Manesis et al . reported that immigrants represented over half of the HDV burden in Greece [ 55 ].

Due to these reasons, HDV is now becoming a serious issue worldwide. A recently published systematic review and meta-analysis reported a worldwide HDV seroprevalence of 14.6% among HBV-positive patients compared with prior estimates of approximately 5%, with a substantially higher seroprevalence in the IVDU and high-risk sexual-behavior populations [ 2 , 88 ]. These findings stress the importance of HDV awareness regardless of country of origin. Indeed, HDV needs to be especially considered in high-risk populations such as among patients who are immigrants from endemic countries, IVDU, MSM and with positive family members.

Diagnostics

This section will focus on the different diagnostic modalities and tests that are available ( Table 2 ). When HDV was first discovered, the diagnosis of HDV relied on immunohistochemical staining of HDAg in liver tissue that could only be obtained through liver biopsy [ 1 ]. Testing for serum immunoglobulin M (IgM)/immunoglobulin G (IgG) anti-HDV quickly became available, which, in addition to liver chemistries and the patient’s clinical picture, enabled classification of patients into the two stages of HDV infection: acute and chronic HDV [ 89 ]. The use of serum IgM/IgG anti-HDV for this purpose was not perfect, however, as anti-HDV IgG is not 100% specific to chronic HDV and can be found in acute HDV. Likewise, anti-HDV IgM is not specific to acute HDV and can frequently be found in chronic HDV [ 61 , 90 , 91 ].

Diagnostic tests for hepatitis D

HDAg, hepatitis D antigen; HDV, hepatitis d virus; RNA, ribonucleic acid; PCR, polymerase chain reaction; LLOD, lower limits of detection; LLOQ, lower limits of quantification.

For more than a decade after the discovery of HDV, testing for the presence of HDV RNA remained sub-optimal, with techniques such as the slot-blot hybridization technique [ 92 ]. In the early 1990s, serum HDV RNA PCR techniques were developed that enabled efficient and accurate testing of HDV in HBsAg-positive patients [ 92–94 ]. However, these early assays only enabled qualitative testing of HDV and were not able to quantify the virus in the serum. The emergence of quantification PCR assays in the early 2000s finally enabled measurement of HDV RNA viremia in the serum [ 95 , 96 ]. Despite these advances, there continued to be a high degree of variation in the sensitivity and specificity of the HDV assays due to a lack of standardization. Recent measures by the World Health Organization (WHO) resulting in the first international external quality control for HDV quantification have led to substantial improvements in this area but significant assay heterogeneity of the available assays remains [ 97 , 98 ].

HDV should be highly suspected in HBV patients with persistently elevated liver chemistries despite suppressed HBV viral loads with or without nucleos(t)ide analog (NA) therapy without a history of significant alcohol intake or metabolic syndrome. This is due to direct suppression of HBV replication by HDV itself [ 48 ]. Not surprisingly, HBV viral loads do not appear to have any correlation with serum alanine aminotransferase (ALT) levels in chronic HDV [ 99 ]. However, this scenario most often applies to hepatitis B envelope antigen (HBeAg)-negative and patients who are HBeAg-positive may still have a high HBV viral load despite the presence of HDV. The American Association for the Study of Liver Diseases (AASLD) currently recommends that HBsAg-positive patients with low or undetectable HBV DNA but high ALT levels be considered for HDV testing while the European Association for the Study of the Liver (EASL) and Asian Pacific Association for the Study of the Liver do not offer specific details regarding which patients with HBV should be tested [ 6–8 ]. The recommended screening test for HDV is serum anti-HDV IgG followed by HDV RNA PCR if positive. Screening is also recommended in HIV-positive patients, IVDU patients, MSM, those at risk for sexually transmitted diseases and immigrants from endemic areas [ 6 ]. Nonetheless, when present, HDV is usually found in the setting of acute hepatitis or chronic liver disease and rarely in the setting of an asymptomatic HBV carrier [ 61 ].

Acute hepatitis D

Acute HDV occurs after an incubation period of 3–7 weeks and may present with non-specific flu-like symptoms with high levels of ALT and aspartate aminotransferase (AST) followed possibly by jaundice [ 100 ]. The presentation of acute HDV can mirror that of acute HBV infection, making it important to test for both processes in a patient with acute hepatitis. Acute HDV can either represent co-infection of HBV and HDV or super-infection of HDV. Co-infection usually leads to an acute self-limited hepatitis that cannot be distinguished clinically from acute HBV. Co-infection induces a cellular immune response followed by down-regulation of HBV replication and elimination of infected hepatocytes by cytotoxic cells [ 101 ]. Meanwhile, super-infection presents as an acute exacerbation of pre-existing chronic HBV or elevations in liver chemistries in an asymptomatic HBsAg carrier [ 100 ]. Acute co-infection of HBV and HDV rarely progresses to a chronic HDV infection, although acute HDV due to super-infection of HDV in a patient with HBV progresses to chronic HDV 80%–100% of the time [ 82 , 101 ].

Clinically, patients may appear the same as in co-infection with elevated ALT levels, but the acute phase of HDV super-infection is characterized by more active HDV replication and suppression of HBV [ 101 ]. In addition to HBV viral loads being markedly suppressed, anti-hepatitis B core (HBc) IgM are usually negative or with low titer [ 46 , 100 ]. Although anti-HDV IgM levels may be a useful indicator of an acute HDV infection, it has only been described to be positive in 41% of acute cases and can also been found during flares of chronic HDV infection [ 61 , 102 ]. Anti-HDV IgG may develop late in acute HDV and may persist for a lifetime even after the patient clears the virus [ 61 , 101 , 102 ].

Acute HDV can vary in severity from mild to fulminant hepatitis. Fulminant hepatic failure has been reported to occur in 1% of HBV/HDV co-infected patients and in 5% of HDV super-infected patients [ 103 ]. Genotype 1 HDV appears to be a risk factor for fulminant hepatic failure in acute HDV due a higher efficiency of editing, assembly and replication compared with genotype 2 [ 31 , 32 , 45 , 104 ]. HDV may cause hepatic failure through direct cytotoxicity caused by the S-HDAg or inducing an exaggerated immune response leading to the destruction of hepatocytes by cytotoxic T cells [ 101 , 105 , 106 ].

Chronic hepatitis D

Chronic HDV is defined as the presence of HDV infection for greater than 6 months. Clinically, patients may be asymptomatic or have non-specific symptoms of fatigue, malaise and anorexia [ 100 ]. Three distinct chronic HBV/HDV patterns have been described. Most patients will have predominant HDV replication with suppressed HBV replication and are HBeAg-negative. This is because HDV tend to suppress HBV transcription as well as HBV virion release, which is hypothesized to be mediated by HDAg [ 107 ]. A similar phenomenon is seen in those with HCV/HDV co-infection as well in which HDV suppresses HCV replication [ 56 ]. In many patients with predominant HDV replication, HBV viral loads may be even undetectable, depending on the sensitivity of the assay. In a cohort of 126 chronic HDV patients, HBV viral loads could not be detected in 67% of patients [ 91 ]. Some HDV patients, however, can have similar viral loads of both viruses and rarely can patients have predominant HBV replication [ 108 ]. These patients are often HBeAg-positive. HBeAg has been reported to be positive in 9.0%–22.8% of HDV cases [ 44 , 45 , 90 , 109 ]. Still, HBV viral loads are not suppressed as much as in the acute hepatitis stage and may reactivate in certain patients [ 46 ].

Chronic hepatitis D outcomes

It is well described that patients who are chronically infected with HBV/HDV have significantly worse liver disease compared to those with chronic HBV mono-infection [ 46 , 101 ]. Table 3 illustrates the increased risks associated with chronic HDV compared with HBV mono-infection. Patients co-infected with chronic HBV/HDV have an accelerated progression to cirrhosis [ 58 , 90 , 110 ], an increased risk of decompensation [ 111 ], an increased risk of HCC [ 58 , 61 , 78 , 90 , 111–113 ], are more likely to undergo liver transplantation [ 48 ] and are at an increased risk for mortality [ 42 , 78 , 90 , 111 ] compared with HBV alone. Co-infections of HCV in addition to HBV/HDV, however, is not a risk factor for more advanced disease [ 56 ]. In the Hepatitis Delta International Network (HDIN) registry of 1576 patients with HDV, cirrhosis was described to be present in 48.7%, HCC developed in 2.5% and 3.6% required liver transplantation [ 44 ]. After cirrhosis develops, the first dominant complication that tends to occur is clinical cirrhotic decompensation and not HCC [ 90 , 111 ].

Associated risks of chronic hepatitis D

Compared with hepatitis B mono-infection.

Interestingly, HBV/HDV-related HCC may be different from HBV mono-infection HCC. Abbas et al . compared HCC in HBV/HDV co-infected patients to those in HBV alone [ 114 ]. HBV mono-infected patients with HCC were more likely to have multifocal tumors, elevations in alpha-fetoprotein level >1000 IU/mL and higher TNM-based staging [ 114 ]. This may be due to a different set of underlying pathogenesis mechanisms driving HBV/HDV HCC compared with HBV HCC. It is thought that HBV causes HCC through mechanisms such as chronic inflammation, integration of HBV DNA into host cellular DNA that disrupt or promote the expression of cellular genes and the direct effect of HBV proteins on cellular functions [ 115 ]. Meanwhile, the underlying drivers of HCC in chronic HDV are thought to be severe necroinflammation resulting in oxidative stress as well as epigenetic mechanisms such as DNA methylation and histone modifications induced by the L-HDAg [ 113 ]. The L-HDAg may also be a mediator in the oxidative stress pathways [ 27 ]. Overall, the risk of HCC in chronic HDV has been described to be increased ∼3- to 6-fold compared with HBV alone [ 58 , 78 , 111 , 112 ]. Like HBV, cirrhotic HDV patients who lose HBsAg and seroconvert to becoming positive for antibody to hepatitis B surface antigen (anti-HBs) with interferon-α (IFN-α) therapy continue to be at risk for HCC [ 90 ].

Although initial studies did not show an association between HDV and mortality [ 61 ], more recent studies have described an increased mortality risk in chronic HDV [ 42 , 78 , 90 , 111 ]. Fattovich et al . demonstrated, in cohort of 2000 Western European HBV-positive patients, that anti-HDV-positive patients were at a 2-fold increased risk of mortality relative to anti-HDV negative HBV patients [ 111 ]. This effect was also seen in a large cohort of HBV/HIV   ±   HDV patients followed for a median of 8.7 years. In this study, Beguelin et al . reported a ∼2-fold increased risk of mortality due to HDV [ 42 ]. The primary cause of death in HDV is most often liver failure [ 90 ]. This finding was supported by Niro et al ., who found that over half of chronic HDV patients who become cirrhotic will advance to liver failure [ 91 ].

Predictors of worse outcomes in chronic HDV have generally varied between studies but have included cirrhosis at presentation [ 82 , 91 ], age [ 44 , 45 , 82 ], male sex [ 91 ], HDV genotype 1 infection [ 45 ], country of origin [ 44 ] and positivity for serum anti-HDV IgM [ 116 ]. Multiple studies have confirmed that the HBV viral load has no impact on meaningful outcomes, although this is possibly due to the suppressive effect of HDV on HBV replication, which prevents any correlation from being obvious [ 45 , 53 , 108 ]. Although HBeAg-positive HDV patients typically have higher biochemical disease activity, HBsAg levels and HBV viral loads compared to HBeAg-negative HDV, long-term clinical outcomes do not differ [ 109 ]. This contrasts with studies in HBV mono-infection that have demonstrated significant associations between HBV viral loads with clinical outcomes such as histology, subsequent risk of cirrhosis and HCC [ 117 , 118 ].

Meanwhile, anti-HDV IgM and HDV RNA levels have been shown to have disease activity and prognostic implications. Anti-HDV IgM levels correlate with higher biochemical activity indicators such as ALT levels as well as total histological activity index [ 90 , 116 ]. In a study of 78 patients from the Hep-Net-International-Delta-Hepatitis-Intervention Trial-2 (HIDIT-2) study with long-term follow-up, only 1 out of 11 (9%) anti-HDV IgM-negative patients developed clinical decompensation compared with 26 of 67 (39%) anti-HDV IgM-positive patients [ 116 ]. Similarly, high HDV RNA levels also correlate with disease activity [ 96 ] and are associated with an increase in the risk of HCC as well as progression to cirrhosis in non-cirrhotic patients [ 90 ]. In genotype 3, HDV RNA levels have been shown to positively correlate with necroinflammatory activity and fibrosis stage and negatively correlate with platelet counts. Patients with an HDV viral load of ≥2log 10 had a significantly increased risk of advanced fibrosis (odds ratio of 6.47; 95% CI, 1.79–23.37; P  =   0.004) [ 108 ].

Therapies for HDV

Although there is currently no US Food and Drug Administration-approved therapy for HDV infection, IFN-α and peg-IFN-α can be used in chronic HDV, although both induce low rates (∼20%–30%) of SVR, defined as an undetectable HDV RNA viral load at 6 months post cessation of treatment [ 36 , 119 , 120 ]. The low rates of response may be due to the interference of HDV with IFN-α intracellular signaling [ 121 ]. Notably, the interpretation of the SVR results of older therapeutic studies in HDV, especially prior to the standardization of the HDV assays by the WHO, should be made with caution, as there are wide variations between the different assays to detect and quantify HDV RNA [ 36 , 97 ]. Additionally, although SVR has been used as the primary outcome in various clinical trials [ 122 , 123 ], there remains uncertainty as to whether this outcome is adequate in HDV due to reported rates of late post-treatment relapse [ 9 ].

A major limitation of IFN-α-based therapies is the known side effects that accompany this therapy, which include; flu-like symptoms, myalgias, arthralgias, exacerbation of psychiatric illness, hematologic toxicity and elevations in transaminases [ 124 ]. Furthermore, the efficacy of IFN-α-based therapy is decreased in cirrhosis and is not recommended for use in patients with advanced cirrhosis (Childs B and C) due to fear of decompensation [ 36 ]. Because of these limitations, many patients with HDV never undergo treatment [ 48 , 90 ]. In a study from Italy, only 30% of patients received interferon therapy with a mean follow-up of 233 months [ 90 ].

Nonetheless, IFN-α-based therapy has been shown to favorably affect the natural history of chronic HDV with substantial benefits that may become evident even years after treatment cessation [ 125 ]. These benefits include improvement of liver histology (specifically activity grade and fibrosis), clearance of HDV, decreased risk of liver decompensation or need for liver transplantation and survival [ 125–127 ]. Prospective data from the Hep-Net Greece Cohort Study showed that interferon-based treatment significantly decreased disease progression in HDV-positive patients (hazard ratio [HR]   =   0.14; 95% CI, 0.02–0.86; P  =   0.033) [ 55 ]. This finding has been collaborated by several other studies that have shown that a lack of interferon therapy was an independent predictor of worse outcome [ 91 ]. Thus, the AASLD recommends peg-IFN-α for 12 months for those with elevated HDV RNA levels and ALT elevation [ 6 ], while EASL recommends peg-IFN-α for at least 48 weeks for those with compensated liver disease [ 7 ].

Interferon-α monotherapy

In chronic HDV infection, two types of IFN-α therapy have been explored: IFN-α2a and IFN-α2b. IFN-α is usually given as a subcutaneous injection three times a week. SVR rates with IFN-α are ∼17% [ 128 ]. In a landmark early study that randomized 42 chronic HDV patients to either IFN-α 9   million units or 3   million units three times a week or no treatment for 48 weeks, 7/14 (50%) of the patients receiving the higher dose of IFN-α had normalization of alanine aminotransferase and clearance of HDV RNA. Treatment with the higher dose was associated with histologic improvement [ 129 ]. However, the high rate of HDV RNA clearance must be interpreted with caution in this study due to the low sensitivities of the assays used at the time as well as the size of the trial.

To improve compliance, a pegylated group was added to IFN-α to form peg-IFN-α that allowed once-a-week subcutaneous dosing [ 128 ]. Like IFN-α, there are two types of peg-IFN-α that have been investigated in trials: peg-IFN-α2a and peg-IFN-α2b, which appear to have similar efficacy. The recommended dose and duration of peg-IFN-α are 180 μg/week for 48 weeks for chronic HDV [ 130 ]. Clinical trials investigating the efficacy of peg-IFN-α are shown in Table 4 . Recent studies have reported SVR rates of approximately 20%–30% after 1   year of therapy with peg-IFN-α [ 122 ]. However, as previously mentioned, relapse is common, even among patients who achieve SVR. In a study evaluating the long-term follow-up of the HIDIT-1 trial, 9 of the 16 patients who achieved SVR tested positive for HDV RNA at least once during post-SVR follow-up [ 9 ].

Clinical trials on the use of pegylated-interferon-α

Peg-IFN-α, pegylated-interferon-α; VR, virological response; SVR, sustained virological response; NR, not reported.

The optimal treatment duration of interferon therapy has continued to be undefined and treatment beyond 1   year is controversial. Although there have been reports of patients who have cleared chronic HDV infection after long-term IFN-α therapy of up to 12 years [ 126 , 134 , 135 ] and a study by Karaca et al ., who reported that more than half of their patients who received peg-IFN-α for 2   years achieved SVR [ 136 ], further studies have shown a lack of substantial improvement in SVR rates or rates of post-treatment relapse [ 135 , 137 , 138 ]. In contrast, a recent retrospective study reported that maintained virological response rates, defined as remaining HDV RNA-negative 2 years after treatment discontinuation, increased with treatment duration and reached 50% at 5 years of treatment [ 127 ].

Interferon combination therapy

Due to the limited efficacy of interferon monotherapy in chronic HDV, several studies have evaluated the utility of combining interferon-based therapy with antiviral medications. Medications that have been studied include: ribavirin [ 131 , 139 ], lamivudine [ 140 , 141 ], famciclovir [ 142 ], tenofovir [ 138 ] and adefovir [ 122 ]. Overall, these studies have not been demonstrated to provide any added benefit such as improvement in virological response rates. The AASLD recommends that, since NAs have no efficacy against HDV, they should not be used in patients with suppressed or low HBV replication except in those with cirrhosis [ 6 ]. Meanwhile, EASL recommends that NA therapy should be considered in HBV/HDV co-infected patients with evidence of ongoing HBV DNA replication (>2000 IU/mL) and can be considered in those with advanced liver disease [ 7 ].

Monitoring for response during and after interferon therapy

During IFN-α or peg-IFN-α therapy, patients should be monitored monthly with complete blood counts and liver chemistries. In addition, patients should be tested for HBsAg and their HDV RNA and HBV DNA should be quantified at baseline and at 3-month intervals during treatment [ 143 , 144 ]. After initiation of peg-IFN-α therapy, HDV RNA begins to decrease at around 1 week [ 145 ]. A negative or greater than 2log 10  IU/mL decline in HDV RNA at 6 months of interferon therapy has been described to be predictive of SVR [ 132 , 146 ]. Early viral kinetics may also predict the likelihood of response to interferon-α-based therapies. Mathematical modeling of HDV viral kinetic responses to peg-IFN-α therapy has demonstrated that HDV declines in a biphasic manner and the presence of a flat second-phase response is associated with non-response [ 145 ]. Additionally, patients with HDV replication greater than 1log 10 higher than HBV replication may have a delayed HDV RNA response to peg-IFN-α therapy [ 147 ]. Finally, HBsAg titers are often correlated with HDV RNA levels and its decline in the serum may be an important early biomarker of HDV response. A HBsAg of less than 1000 IU/mL at 6 months is predictive of HDV loss [ 135 , 148 ].

Investigational therapies

Due to the current limitations of interferon-α-based therapies, there has been substantial recent interest in novel therapies for this devastating disease. Current investigational therapeutic pipelines can be separated into the following classes: (i) interferon-lambda (IFN-λ), (ii) prenylation inhibitors (Lonafarnib [LNF]), (iii) entry inhibitors (Myrcludex B) and (iv) nucleic acid polymers (NAPs). These new therapies target various stages of the HDV life cycle and are currently in various stages of clinical development, with promising results thus far ( Figure 1 and Table 5 ). RNA-interference (RNAi)-based therapies that target post-transcriptional gene silencing are also on the horizon for HDV but have yet to undergo clinical testing [ 158 , 159 ]. Of note, clinical trials with the new investigational therapies have explored a variety of new outcomes compared with older trials. A decline of greater than 2log 10  IU/mL of HDV RNA was recently proposed as a surrogate marker for initial treatment efficacy [ 160 ].

Clinical trials on investigative treatments for hepatitis D

Post-treatment result.

Interim results; peg-IFN-λ, pegylated-interferon-λ; HDV, hepatitis D virus; LNF, lonafarnib; TDF, tenofovir disoproxil fumarate; NR, not reported; RTV, ritonavir; LOWR, LOnfarnib With and without Ritonavir; MB, Myrcludex B; pegylated-interferon-α, peg-IFN-α.

Pegylated-interferon-lambda

Pegylated-interferon-lambda-1a (peg-IFN-λ) is a conjugate of the recombinant human type-III IFN, IL-29 and a linear polyethylene glycol chain that has antiviral activity against HBV and HCV like peg-IFN-α, which is a type-I IFN [ 161 ]. However, unlike type-I IFN receptors, which are ubiquitously expressed in all tissues and cells, type-III IFN receptors are only restricted to cells of epithelial origin and theoretically more heavily concentrated in the liver. Due to this, IFN-λ has been described to cause fewer systemic interferon side effects such as myalgias, flu-like symptoms and arthralgias, thus improving tolerability [ 162 ]. However, the two interferons act on the same interferon-stimulated-genes pathway that acts on the JAK/STAT signal-transduction cascade, leading to antiviral activities and reduction of HDV viremia as well as intrahepatic genomic and antigenomic HDV RNA [ 161 , 163 ].

Since peg-IFN-λ has a better tolerability profile compared with peg-IFN-α, it has been investigated in HBV (with comparable efficacy to peg-IFN-α) [ 164 ], HCV [ 165 ] and now HDV [ 149 ]. In HDV, the LIMT-HDV ( L ambda I nterferon M ono T herapy in H epatitis D elta V irus) study [NCT02765802] is a phase 2, open-label, randomized study evaluating two doses of peg-IFN-λ (120 and 180 mcg weekly) in 33 patients with HDV for 48 weeks. Interim results reporting data on the first 20 patients have been encouraging. By Week 8, 3 of 11 patients had become HDV RNA-negative and 5 of 11 had a greater than –2log 10  IU/mL decline in HDV RNA [ 149 ]. End-of-trial data from that study are pending, although another clinical trial called the LIFT ( L ambda I nter F eron combo T herapy) trial [NCT03600714] recently started enrolling at the National Institutes of Health. This trial is investigating combination therapy with peg-IFN-λ, LNF and ritonavir (RTV) in 26 patients for 24 weeks.

Prenylation inhibitors (Lonafarnib)

As described earlier, prenylation is the process of adding a prenyl lipid group (either farnesyl or geranylgeranyl) to the C-terminal cysteine of the target protein [ 29 ]. In HDV, a farnesyl group is added to the C-terminus of the L-HDAg in a process called farnesylation catalysed by the enzyme farnesyltransferase [ 15 ]. This host process is critical to viral assembly, as it causes the L-HDAg to become lipophilic and join with the HBsAg to form a virus particle that is ready to be secreted and infect other hepatocytes [ 166 ]. LNF is an oral prenylation inhibitor that acts on the enzyme farnesyltransferase ( Figure 1 ) [ 167 ]. In mouse and hepatic tissue-culture studies, it has been shown to inhibit the secretion of virions and leads to intracellular accumulation of viral RNA, prevent production of infectious HDV particles and enhance the innate immune response [ 166 , 168 ]. LNF has been studied in various malignancies including progeria and thus has a proven safety record [ 169 , 170 ]. To date, LNF has been studied in over 100 patients with chronic HDV [ 150–154 ].

In a seminal proof-of-concept, phase 2 A double-blinded, randomized, placebo-controlled study, LNF was tested in 14 patients with chronic HDV infection at doses of 100 mg (Group 1) and 200 mg (Group 2) twice daily for 28 days with 6 months of post-therapy follow-up [ 150 ]. Patients experienced a mean log HDV RNA decrease of 0.73log 10  IU/mL (Group 1) and 1.54log 10  IU/mL (Group 2). Half of the patients in Group 2 achieved a decrease from baseline to nadir HDV RNA of greater than –2log 10  IU/mL. Serum LNF concentrations correlated with HDV RNA changes ( r 2   =   0.78; P  <   0.001). This study provided the first evidence that another therapy, other than interferon, had efficacy in chronic HDV. However, gastrointestinal side effects such as diarrhea, nausea, anorexia, dyspepsia and weight loss were common, especially among patients in the higher-dose group, and the HDV RNA suppression was not sustained after discontinuation of therapy.

Subsequently, this trial was followed by four dose finding/optimization clinical trials termed LOWR-HDV ( LO nafarnib W ith R itonavir in H DV) 1, 2, 3 and 4 [ 151–154 ]. Since LNF is extensively metabolized by CYP3A4, these clinical trials included the addition of RTV—a CYP3A4 inhibitor that has been extensively used in HIV [ 171 ]. By utilizing RTV, LNF levels could be boosted in the blood while the gastrointestinal tract was exposed to lower doses of LNF. This allowed lower doses of lonafarnib, resulting in better tolerability while simultaneously increasing post-absorption LNF levels and antiviral efficacy [ 172 ].

LOWR-1 [NCT02430181] was a single-center, phase 2 pilot study performed in Ankara, Turkey that investigated varying doses of LNF   ±   RTV   ±   peg-IFN-α for 5–12 weeks in five groups of patients (three patients per group) [ 151 ]. The most impressive antiviral and biochemical responses were achieved in the LNF 100 mg twice daily (BID)   +   RTV 100 mg daily (HDV decline 3.2log 10   IU/L) and LNF 100 mg BID   +   peg-IFN-α groups (HDV decline 3.0log 10   IU/L) after 8 weeks of therapy. The rate of decline was more rapid compared with prior studies with peg-IFN-α alone [ 122 ]. Although no patients cleared the virus during treatment, two patients in the LNF monotherapy group achieved an undetectable HDV viral load post treatment after a transient ALT flare [ 151 ].

LOWR-2 [NCT02430194] was a phase 2, dose-ranging study that attempted to optimize dosing by evaluating 58 patients treated with 10 separate treatment arms of LNF (25 mg, 50 mg, 100 mg BID)  + RTV 100 mg BID ± peg-IFN-α for 12–24 weeks [ 173 ]. This study showed impressive synergistic activity of lower-dose LNF/RTV with peg-IFN-α resulting in an HDV decline of 5.57log 10   IU/L at 24 weeks. Three of five patients became HDV RNA-negative and ALT-normalized, and the regimen was well tolerated [ 152 ]. Interestingly, from the LOWR-1 and LOWR-2 studies, 5 of 27 (18.5%) patients treated with LNF who had a detectable HDV RNA at the end of treatment subsequently experienced a post-treatment ALT flare followed by rapid clearance of HDV, suggesting immune restoration [ 174 ].

LOWR-3 [NCT02511431] is a phase 2, double-blind, randomized, placebo-controlled study that evaluated once-daily dosing in 21 patients for 12–24 weeks [ 153 ]. Patients were randomized to doses of LNF at 50, 75 or 100 mg plus RTV 100 mg once a day. Final data are pending but patients experienced the highest HDV decline with LNF 50 mg (1.93log 10   IU/L) compared with LNF 75 mg (1.3log 10   IU/L) and LNF 100 mg (0.29log 10   IU/L) at 24 weeks. One patient became HDV RNA-negative during the study and 6/21 (28.6%) patients achieved a HDV RNA below 250 IU/mL [ 153 ].

Finally, LOWR-4 [NCT02527707] is a phase 2, open-label, dose-titration study that treated 15 chronic HDV patients for 24 weeks [ 154 ]. Patients were started on LNF 50 mg BID and RTV 100 mg BID initially. LNF was then increased to a maximum of 100 mg BID per protocol as tolerated. Interim results have been reported describing that dose escalation was feasible and patients experienced a mean HDV decline of 1.87log 10   IU/L at Week 8 [ 154 ].

In summary, the regimen that appears to have the highest efficacy in these LOWR-HDV trials is that of low-dose LNF 25 or 50 mg twice a day and ritonavir 100 mg twice a day with peg-IFN-α from LOWR-2. Three of five patients were HDV RNA-negative at Week 24—a response that persisted to Week 48 in the two patients who stopped treatment at Week 24 [ 175 ]. Although these results are promising and LNF has been well tolerated in the recent LOWR trials, long-term follow-up regarding therapy efficacy and safety are needed. It is encouraging to note that there has not been any evidence of viral resistance in the LNF studies thus far [ 151–154 ]. As mentioned, the LIFT trial [NCT03600714] evaluating the combination of peg-IFN-λ, LNF and RTV is ongoing. A phase 3 trial called the D-LIVR ( D elta L iver I mprovement and V irologic R esponse) study [NCT03719313] studying the efficacy and safety of LNF + RTF ± peg-INF-α will begin recruiting soon.

Entry inhibitor (Myrcludex B)

Myrcludex B is a myristoylated peptide of 47-amino acids derived from the preS1-domain of the L-HBsAg protein and first-in-class HBV/HDV entry inhibitor that works by inactivating the host receptor, NTCP [ 20 ]. This receptor is crucial for viral entry and inactivation leads to a decrease in the number of infected cells ( Figure 1 ). Entry inhibitors as a class may also have a role in eliminating intrahepatic HBV/HDV genome [ 176 ]. Initial mice studies of Myrcludex B showed that Myrcludex B significantly inhibited HDV-infection establishment. However, continuous drug administration was necessary to prevent HDV spread [ 177 ].

In a phase 1 b/2a, randomized, three-arm, parallel, open-label, proof-of-concept study [NCT02637999] evaluating 24 patients with chronic HDV randomized (1:1:1) to Myrcludex B, peg-IFN-α or combination, Myrcludex B for 24 weeks showed efficacy as both a monotherapy as well as exhibiting a synergistic effect with peg-IFN-α. Myrcludex B was administered as a 2-mg subcutaneous injection once daily. Although the primary endpoint—a change in HBsAg levels—was not met, both Myrcludex B monotherapy and combination therapy with peg-IFN-α led to significant declines in HDV RNA and ALT levels. At 24 weeks, mean HDV declines were as follows: 1.67log 10   IU/L (Myrcludex B), 2.6log 10   IU/L (Myrcludex B + peg-IFN-α) and 2.2log 10   IU/L (peg-IFN-α). Two out of the eight patients in both monotherapy groups became HDV RNA-negative, while combination therapy led to five of the seven patients becoming HDV RNA-negative [ 155 ]. Myrcludex was generally well tolerated.

This study was followed by a phase 2 b, multicenter, open-label study [NCT03546621] conducted in 120 patients with chronic HDV who were randomized to tenofovir ± Myrcludex B (2, 5, 10 mg) for 24 weeks. At 24 weeks, HDV declines were the most impressive at 5 and 10 mg: 1.6log 10   IU/L (Myrcludex B 5 mg) and 2.7log 10   IU/L (Myrcludex B 10 mg) [ 156 , 178 ]. Efficacy was dose-dependent, with the best results seen at the 10-mg dose, with 76.6% of the patients in that arm achieving the primary endpoint (a decrease in HDV RNA by 2log 10 or HDV RNA negativity). However, relapse occurred in most responders (60%–83%, depending on group) after cessation of therapy [ 156 ]. A phase 2, randomized, open-label study [NCT02637999] evaluating Myrcludex B ± peg-IFN-α for 24 weeks followed by peg-IFN-α for 48 weeks vs peg-IFN-α for 48 weeks has been completed, with results pending.

Although these results are promising, the appearance of antibodies to Myrcludex B in some patients has been described and is likely to be concerning. Although no correlation between the appearance of antibodies to safety or efficacy has been seen, attention to this finding has to be made in future studies [ 155 ]. In addition, HDV has been shown in ‘ in vitro ’ and ‘ in vivo ’ studies to propagate during liver regeneration through clonal cell division despite the presence of Myrcludex B [ 179 ]. Furthermore, Blank et al . reported that Myrcludex B significantly increases total plasma bile-acid exposure by 19.2-fold and conjugated bile acids by 124-fold in healthy human volunteers because NTCP is also a physiological bile-acid transporter [ 180 ]. Although the patients in that study remained asymptomatic, the long-term effects of elevated bile acids in the setting are unknown [ 180 ].

Nucleic acid-based polymer (REP2139)

NAPs are phosphorothioated oligonucleotides with broad-spectrum antiviral activity against many different types of viral infections including HCV and HIV [ 181–184 ]. NAPs continue to be investigated in HBV monotherapy due to a potent effect on HBsAg secretion [ 185 , 186 ]. The leading drug in this class of HDV medication is REP2139 (Replicor©), which is administered as a once-a-week intravenous infusion. In HDV, the exact mechanisms of antiviral effects of NAPs have yet to be fully elucidated, but they appear to inhibit the secretion of HBsAg envelope proteins as well as being active at viral entry ( Figure 1 ) [ 185 , 187 ]. The antiviral effects of NAPs appear to be dependent on the size and amphipathicity of the polymer. The inhibition of viral entry of NAPs appears to be at least partly due to the NAPs binding to HDV particles and preventing attachment of the virus to the cell-surface glycosaminoglycans [ 181 ].

The initial proof-of-concept study, REP301 [NCT02233075], was an open-label, non-randomized study evaluating 12 patients with chronic HDV [ 157 ]. Patients received 500 mg intravenous REP2139 weekly for 15 weeks followed by combination therapy of 250 mg intravenous REP2139 and peg-IFN-α for 15 weeks and then peg-IFN-α monotherapy for 33 weeks. REP2139 demonstrated potent efficacy on HBV and HDV. There was a mean 3.5log 10   IU/L decline in HBsAg from baseline and 5 of 12 patients became HBsAg-negative, which was maintained to 1 year post treatment. Nine of 12 patients became HDV RNA-negative by the time of treatment, with 7 of 9 patients remaining HDV RNA-negative at 1.5 years of post-therapy follow-up. Mean HDV RNA decline was 5.34log 10   IU/L [ 157 , 188 ]. Durability of the response is being evaluated in a long-term follow-up study [NCT02876419].

REP2139 appears to be the only one of the new investigative drugs that results in a fast reduction in HBsAg [ 143 ]. Although REP2139 was well tolerated, substantial ALT flares did occur in some patients, which may limit its use in cirrhosis [ 187 ]. Other concerns with NAPs include: side effects such as hair loss, dysphagia and dysgeusia that were seen during a prior HBV trial, which was attributed to heavy-metal exposure at the trial site, as well as the possibility of late relapses, which were seen during a prior HBV trial [ 157 , 185 ].

HDV is a rapidly progressive viral hepatitis that increases the risk of cirrhosis, HCC, hepatic decompensation, liver transplantation and mortality compared with HBV mono-infection. Due to immigration and improvements in diagnosis through the development and standardization of diagnostic tests, HDV is now becoming increasingly recognized as a problem worldwide. However, there continues to be a lack of efficacious treatment options. Interferon therapy with peg-IFN-α remains the only regularly used therapy outside of clinical trials. However, recent improvements in our understanding of the virus have led to the investigation of several new and promising therapies—one or more of which may eventually be approved for use in HDV.

B.D. and C.K. conceived of and designed the manuscript. B.D. and C.K. interpreted the available studies on the subject. B.D., T.H. and C.K. drafted and revised the manuscript. All authors reviewed and approved the final manuscript.

This study was supported by [grant number Z99-DK-999999] from the Intramural Research Programs of the National Institute of Diabetes and Digestive and Kidney Diseases.

Conflict of interest

None declared.

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Bazinet M , Pantea V , Cebotarescu V et al.  Establishment of persistent functional remission of HBV and HDV infection following REP 2139 and pegylated interferon alpha 2a therapy in patients with chronic HBV/HDV co-infection: 18 month follow-up results from the REP 301-LTF study . J Hepatol 2018 ; 68 : S509.

• liver cirrhosis
• epidemiology
• hepatitis b
• hepatitis d
• hepatitis b surface antigens
• infectious mononucleosis
• interferons
• life cycle stages
• hepatitis b virus
• human leukocyte interferon
• experimental treatment

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Hepatitis is an inflammation of the liver that is caused by a variety of infectious viruses  and noninfectious agents leading to a range of health problems, some of which can be fatal. There are five main strains of the hepatitis virus, referred to as types A, B, C, D and E. While they all cause liver disease, they differ in important ways including modes of transmission, severity of the illness, geographical distribution and prevention methods. In particular, types B and C lead to chronic disease in hundreds of millions of people and together are the most common cause of liver cirrhosis, liver cancer and viral hepatitis-related deaths. An estimated 354 million people worldwide live with hepatitis B or C, and for most, testing and treatment remain beyond reach.

Some types of hepatitis are preventable through vaccination. A WHO study found that an estimated 4.5 million premature deaths could be prevented in low- and middle-income countries by 2030 through vaccination, diagnostic tests, medicines and education campaigns. WHO’s global hepatitis strategy, endorsed by all WHO Member States, aims to reduce new hepatitis infections by 90% and deaths by 65% between 2016 and 2030.

Many people with hepatitis A, B, C, D or E exhibit only mild symptoms or no symptoms at all. Each form of the virus, however, can cause more severe symptoms. Symptoms of hepatitis A, B and C may include fever, malaise, loss of appetite, diarrhoea, nausea, abdominal discomfort, dark-coloured urine and jaundice (a yellowing of the skin and whites of the eyes). In some cases, the virus can also cause a chronic liver infection that can later develop into cirrhosis (a scarring of the liver) or liver cancer. These patients are at risk of death.

Hepatitis D (HDV) is only found in people already infected with hepatitis B (HBV); however, the dual infection of HBV and HDV can cause a more serious infection and poorer health outcomes, including accelerated progression to cirrhosis. Development of chronic hepatitis D is rare.

Hepatitis E (HEV) begins with mild fever, reduced appetite, nausea and vomiting lasting for a few days. Some persons may also have abdominal pain, itching (without skin lesions), skin rash or joint pain. They may also exhibit jaundice, with dark urine and pale stools, and a slightly enlarged, tender liver (hepatomegaly), or occasionally acute liver failure.

Safe and effective vaccines are available to prevent hepatitis B virus (HBV). This vaccine also prevents the development of hepatitis D virus (HDV) and given at birth strongly reduces transmission risk from mother to child. Chronic hepatitis B infection can be treated with antiviral agents. Treatment can slow the progression of cirrhosis, reduce incidence of liver cancer and improve long term survival. Only a proportion of people with chronic hepatitis B infection will require treatment. A vaccine also exists to prevent infections of hepatitis E (HEV), although it is not currently widely available. There are no specific treatments for HBV and HEV and hospitalization is not usually required. It is advised to avoid unnecessary medications due to the negative effect on liver function caused by these infections.

Hepatitis C (HCV) can cause both acute and chronic infection. Some people recover on their own, while others develop a life-threatening infection or further complications, including cirrhosis or cancer. There is no vaccine for hepatitis C. Antiviral medicines can cure more than 95% of persons with hepatitis C infection, thereby reducing the risk of death from cirrhosis and liver cancer, but access to diagnosis and treatment remains low.

Hepatitis A virus (HAV) is most common is low- and middle-income countries due to reduced access to clean and reliable water sources and the increased risk of contaminated food. A safe and effective vaccine is available to prevent hepatitis A. Most HAV infections are mild, with the majority of people recovering fully and developing immunity to further infection. However, these infections can also rarely be severe and life threatening due to the risk of liver failure.

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Hepatitis B infection: An overview

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Hepatitis, one of the major incurable diseases, still exists nowadays endangering many people’s lives. It has many types i.e. Hepatitis A, B, C, D, E and G. The nature of Hepatitis is viral which is caught by either through body fluids or improper personal hygiene in addition to other causes which remains unknown.

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Hepatitis - Free Essay Examples and Topic Ideas

Hepatitis is a liver disease caused by a virus, which can range from mild to severe. The most common types are hepatitis A, B, and C, which are spread through contaminated food, water, or bodily fluids. Symptoms include fatigue, nausea, stomach pain, and jaundice. Vaccines are available for types A and B, and treatments are available for type C. Chronic hepatitis can lead to liver damage, cirrhosis, and even liver cancer. It is important to seek medical attention if symptoms are present or if at risk for contracting hepatitis.

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• Hepatitis A
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Hepatitis B Virus (HBV)

Show More The core of the hepatitis B virus is generally in the shape of an icosahedron. Within the virus, there are two strands of DNA, one smaller than the other, which is circular. HBV is around 42 nm in width, and the core is surrounded in a 4nm thick coat. They are enveloped, which means they are more susceptible to being destroyed, because the envelope is very thin. Viruses in general are very small, much smaller than bacteria, and HBV is no different. (Image: commons.wikimedia.org) Reproduction The hepatitis B virus reproduces in the same way as most (if not all) other viruses do. It attaches itself to the host cell and injects its own genetic material into the nucleus of the cell. The host cell is used to make copies …show more content… As the virus is transmitted by infected bodily fluid, and gets into the body directly (such as a needle being injected into the skin), the main function of the first defence is to create a barrier so that only a minimal amount of the virus enters. The second line of defence is also non-specific, so cannot kill the virus alone. When the immune system tires to kill off HBV, it also damages the liver cells, because the cells involved in this process are not designed to specifically target the invader. In some cases, the inflammatory process can kill not only the virus but also the liver, and therefore the person who was infected. However, death by HBV is rare, more common in adults than children, and only occurs when the carrier has chronic hepatitis B. This can be treated to an extent. The third line of defence (as mentioned in the bacteria section of this report), is where T-Cells and B-Cells partner together to detect and destroy specific cells. This is the most effective defence, and if the immune system of the infected person works to kill the virus, no medication should be required (this would be an acute case of …show more content… Treatment such as antiviral medication is available to stop help stop the virus from continuing to replicate and spread, and to fight the virus’ effects (i.e. stop the virus from damaging the liver further). Another option for infected persons is a liver transplant, where the damaged liver is removed and replaced with a healthy one. There are other drugs that are being developed as well, aimed at treating hepatitis B effectively. Currently, there is no way to cure a person of the infection fully, merely the above ways of preventing others from getting infected and decreasing the damage the infection can

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Hepatitis B I Can't Believe

The doctor said that I'm pretty healthy now, although I was bedridden for about two weeks during which time I changed my diet substantially to eat more fruits and vegetables and less red meat per the advice of the physician. I have also substantially increased my fluids intake -- I now drink eight glasses of water a day. The physician told me that for someone with my degree of health, the main thing is to attempt to prevent any further inflammations or flare up of this virus. He said that as long as I continue to maintain my health, the only things we have to do is carefully monitor my liver, primarily with blood tests, and to stay cognizant of any other potential hazardous effects to related bodily functions (Dugdale, 2010). That way I can avoid anything drastic, such as the need for a liver transplant. Although the acute stage…...

mla References Dugdale, D.C. (2010). "Hepatitis B" PubMed Health. Retrieved from   http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001324/  World Health Organization. (2012). "Hepatitis B" Global Response Alert. Retrieved from   http://www.who.int/csr/disease/hepatitis/whocdscsrlyo20022/en/index1.html#who

Hepatitis B Is the Known

(Kanwal et al.) However, it has been found that in many cases alternative strategies to medication are often more effective. The following are a list of commonly prescribed drugs as approved by the FDA and their wholesale prices as of 2005. Lamivudine (100 mg) - monthly cost $204- annual cost $2,482 Adefovir (10 mg) - monthly cost $546 - annual cost $6,647 Entecavir (0.5 mg) - monthly cost $715 - annual cost $8,694 Peginterferon alfa-2a (180 mcg) - monthly cost -$1,540 - annual cost $18,480 Emtricitabine (200 mg) - monthly cost $318 - annual cost $3,872 Tenofovir (300 mg) - monthly cost $478 - annual cost $5,811 ( Hepatitis B Foundation, B Informed Newsletter, No. 46, Summer 2006) eferences Approved Drugs for Adults. July 17, 2009. Kanwal et al. Treatment Alternatives for Chronic Hepatitis B Virus Infection: A Cost- Effectiveness Analysis. Annals of Internal Medicine. Vol. 142, 10. July 17, 2009. Hepatitis. July 17, 2009. Hepatitis B July 17, 2009. Hepatitis B: Brown.Edu.…...

mla References Approved Drugs for Adults. July 17, 2009. Kanwal et al. Treatment Alternatives for Chronic Hepatitis B Virus Infection: A Cost- Effectiveness Analysis. Annals of Internal Medicine. Vol. 142, 10. July 17, 2009.

Hepatitis B

Hep B The Causative Agent Hepatitis is a viral infection of the liver. The primary microbe responsible for the manifestation of the disease is the Hepatitis B virus (HBV), which is a member of the hepadnavirus family. Other members of the hepadnavirus family affect both birds and small mammals including squirrels and woodchucks, but humans are the only known mammals to be susceptible to Hepatitis B in particular (Hepatitis B; McLachlan, 1991). Hepadnaviruses are double-stranded and double-shelled DNA. The Hepatitis B virus itself is only 42-nm with an electron-dense core of 27 nm (Zuckerman, 1996). It has a small genome but also has many antigenic compounds including HBsAg, HBcAg, and HBeAg. It is therefore highly resilient and can remain without a host for up to one week (Hepatitis B). Moreover, the hepatitis B virus replicates with reverse transcription, which is unusual (Zuckerman 1996). Demographics, Morbidity and Mortality About 2 billion people worldwide have been…...

mla References Blumberg, BS. 2002. The hunt for a killer virus. Princeton: Princeton University Press. Hepatitis B In: Green Book Chapter 18, v. 2. Available online:   https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/263311/Green_Book_Chapter_18_v2_0.pdf  Hepatitis B In: Pink Book. CDC. Available online:   http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/hepb.pdf  McLachlan, A. 1991. Molecular biology of the hepatitis virus. CRC Press.

Hepatitis B Virus Hbv Infection

7. The limitations of the study are minimal, including only the fact that the study demonstrates only minimal literature review and would be strengthened by such review, specific to Uganda and not only inclusive of the whole of the region or the whole of Africa. This may be in part due the severely limited set of research information from which to pull from, but if so this is not explained in the work but must then be assumed by the reader. 8. This work is generalizable but it could be challenging to develop the behavior review aspect of the study among different populations due to compliance and privacy issues. Yet, with the assurance of anonymity the study could be repeated and would be helpful elsewhere, where HBV is endemic. The research study might also be better served if it is conducted among other medical and medical support professionals in the nation…...

mla Works Cited Pido, Bongomin & Kagimu, Magid Prevelence of Hepatitus B virus (HBV) Infection Among Makerere University Medical Students. African Health Sciences, 5(2) June 2005, 93-98.

Hepatitis B Realities Revealed

Hepatitis B There are a couple of different concerns for public health pertaining to Hepatitis B. Probably the most salient of these relates to the fact that this condition can be transferred amongst people via unprotected sexual activity. In this respect, this condition is just one of the many that people can incur through unsafe sex. Additionally, public health concerns related to Hepatitis B revolve around the fact that contact with an infected person's blood can infect others. Thus, health care practitioners must be extremely careful when treating people with this condition. Finally, sharing items for personal hygiene and needles is a point of concern for patients with Hepatits B, because such sharing is another way in which this disease is transferable. The chain of this infection can be interrupted in a couple of different ways. Perhaps one of the most important of these is to treat this condition and stop…...

mla References Hepmag. (2010). Hepatitis B: the basics. www.hepmag.com Retrieved from   http://www.hepmag.com/articles/2511_18747.shtml  Ma, G., Gao, W., Tan, Y., Chae, W., Rhee, J. (2012). A community-based participatory approach to a hepatitis B intervention for Korean-Americans. www.ncbi.nlm.nih.gov / Retrieved from   http://www.ncbi.nlm.nih.gov/pubmed/22643783  World Health Organization. (2015). WHO issues its first hepatitis B treatment guidelines. www.who.int / Retrieved from   http://www.who.int/mediacentre/news/releases/2015/hepatitis-b-guideline/en/

Hep B Hepatitis B This

This implies a crisis for the Asian community in proportion to the AIDS epidemic. The medical community erroneously has been the typical Caucasian model for the diagnosis and treatment which entails that Asians are the same make up as Caucasians. The hepatitis B virus has been rampant in Asia and a large percentage of mothers pass it on to their children during birth. Although the virus infects males and females equally, it usually kills Asian males more often through the inherent cancer or liver disease. Asian children grow up healthy because the dormant virus hides in the liver and unleashes its destructive power during young adulthood. Therefore, Asian men in their 20's or 30's are at a high risk for liver cancer. Unfortunately, being born in the United States as opposed to Asia has not made a difference in the Asian population. The serological results presented help to provide insights…...

Educating the Stakeholders to Eliminate Transmission of Hepatitis B

Epidemiological Aspects of Hepatitis B in Community-Based Health Educating About Hepatitis B Overview of Hepatitis B Epidemiology Hepatitis B is caused by infection with the Hepatitis B virus (HBV) ("CDC," 2012). The highest concentrations of HBV are found in blood, while other body fluid, such as semen, vaginal secretions, and wound exudates, show lower concentrations ("CDC," 2012). HBV infection can be either chronic or self-limited ("CDC," 2012). The incubation period can range from 6 weeks to 6 months from the time of initial exposure to the onset of symptoms ("CDC," 2012). oughly half of newly acquired HBV infections in adults are symptomatic. Acute liver failure and eventual death occurs in 1% of all reported cases ("CDC," 2012). The age of infection shows an inverse relationship to chronic infection. Accordingly, 2 to 6% of adults suffer from chronic infection, while 30% of children five years and under and 90% of infants become chronically infected ("CDC,"…...

mla References Centers for Disease Control and Prevention (CDC) Hepatitis B Information for Health Professionals. [Web] Retrieved  

Communicable Disease Hepatitis B

epidemiology nursing research a communicable disease. Communicable isease Selection Choose communicable disease list: 1. Chickenpox 2. Tuberculosis 3. Influenza 4. Communicable diseases according to (Copstead & Banasik, 2010) is a condition or infection that is transmissible through coming into contact with an infected person. Contact with the infected person comprises of contact with an infected person bodily fluids (blood, saliva, or mucus), droplets, and/or air or food (Copstead & Banasik, 2010). Coming into contact in any of the above ways contributes to individual's illness. The pathogens transmitted through the body fluids and air encroaches upon the body compromising the normal functioning of body cells. This compromise may have differing impacts upon an individual's health ranging from a terminal illness to death. Hepatitis BCommunicable isease: Hepatitis B Communicable diseases are diseases that can be transmitted via contact, droplet, air/food borne, blood, bodily fluids or congenital infection and cause individuals to become ill. The…...

mla Demographics Approximately 60,000 people die every year from HBV (WHO, 2013). There are about 200 billion people living around the world with HBV with an estimated 1.2 million living in the United States (CDC, 2013). In 2011, the United States was estimated to have 18,800 actual new cases of the HBV (CDC, 2013). Those who are at greatest risk for developing HBV are Asian and Pacific Islanders, African-Americans, gay and bisexual individuals, those who have multiple sex partners and do not practice safe sex or are intravenous drug users. Gay and bisexual men make up 20% of new HBV cases and 50% Asian and Pacific Islanders are living with HBV (CDC, 2013). Most Asian and Pacific Islanders were infected with HBV as infants or children and 1 in 12 are living with it and are not even aware. According to 2013 World Health Organization's publication, approximately sixty thousand people die every year due to HBV infections. In the globe, an estimate of about two billion persons are infected with 1.2 million of this [persons living in the United States (World Health Organization, 2013). Individual at the greatest risk of acquiring HBV infections include; African-Americans, Asian, Pacific Islanders, bisexual and gay individuals. Additional to the persons

Immunology Hepatitis B And C

The surgeon had admitted to applying hemostatic material to sternal incisions without the use of sponges, which is not recommended due to the possibility of glove tears and percutaneous contact. Therefore, there is atleast some evidence for 'inadequate infection control'. However, it must be added that the rare percutaneous exposure does not account for the high rate of infection as identified in this study. Since it is well-known that H infections tend to be asymptomatic in almost 70% of the cases, it increases the risk factor of the physician transmitting the virus unknowingly. [3] Health care workers (HCW) who perform invasive procedures are obligated to know their serological status for HIV, H and other chronic infectious conditions. Medical practice of HeAg-positive health care worker should be carefully monitored and restricted as the health Canada panel recommended recently. [4] latant or negligent violations in this respect, on the part of the…...

mla Bibliography 1) Gerlich WH, 'Hepatitis B and C. Risk of transmission from infected health care workers to patients' Bundesgesundheitsblatt Gesundheitsforschung Gesundheitsschutz., 2004 Apr;47(4):369-78 2) Rafael Harpaz MD & Lorenz Von Seidlein et.al, 'TRANSMISSION OF HEPATITIS B VIRUS TO MULTIPLE PATIENTS FROM A SURGEON WITHOUT EVIDENCE OF INADEQUATE INFECTION CONTROL',

Importance of Hepatitis B Screening for Health Care Workers in Primary Health Care

Hepatitis B screening for health care workers in primary health care The cause for Hepatitis B is a DNA virus and the complete virus has the name 'Dane particle'. The virus contains three major antigens in structure: The surface antigen, the core antigen and e antigen. Hepatitis B is more prevalent among certain population groups and this group contains the health care workers also. (Hepatitis B Seronegative Commonalties in Health Care Workers. Seronegative Commonalties). The susceptibility for health care workers exists for a variety of infections due to the nature of their work. All workers for health care like physicians, nurses, emergency medical personnel, dental professionals and students, medical and nursing students, laboratory technicians, hospital volunteers and even administrative staff are at risk due to their regular contact with patients and their infected material. These diseases are preventable with suitable vaccines. It is thus very important to maintain immunity for…...

mla References Duties of Care" (1998) Retrieved at   (Accessed: 2004, 16 August) http://www.safetyline.wa.gov.au/institute/level2/course20/lecture81/l81_07.asp  General Health Encyclopedia: Hepatitis B" Retrieved at   (Accessed: 2004, 16 August) http://www.healthcentral.com/mhc/top/000279.cfm  Hepatitis B" Retrieved at (Accessed: 2004, 16 August) http://cancer-symptoms.org/hepatitis-b.htm Hepatitis B" Retrieved at   (Accessed: 2004, 16 August) http://www.cpmc.org/advanced/liver/patients/topics/hepb.html 

Developing Culturally Sensitive Interventions for Hepatitis B

Bastani, R., Glenn, B. A. et al. (2014, May 1). Developing theoretically based and culturally appropriate interventions to promote hepatitis B testing in 4 Asian-American populations, 2006-2011, Preventing Chronic Disease, 11. DOI: http://dx.doi.org/10.5888 / pcd11.130245. Identify the health behavior theory used in this article According to Maxwell et al. (2014), this study used a health behavior framework that was a synthesis of several major theories concerning health behavior. Identify the level of intervention targeted by the intervention (individual, interpersonal, community) he intervention of this study was at the community level for selected Vietnamese, Cambodian and Hmong populations. Identify the intervention strategy used in this article and provide your assessment of its appropriateness o their credit, Maxwell and her associates (2014) used intervention strategies that were specifically designed to ensure maximum coverage of the targeted populations in an effort to promote hepatitis B testing in community settings rather than clinical settings due to their paucity of regular…...

mla The novel health behavior framework developed by Maxwell et al. (2014) was comprised of the constructs that were most relevant for hepatitis B testing that were identified through a systematic review of the literature. In this regard, Maxwell et al. (2014) report that, "We reviewed intervention programs that had been implemented successfully in the population in the past. These factors guided the overall intervention approach in each group (e.g., mass media, home visits by lay health workers)" (p. 2). Based on these findings, Maxwell and her associates (2014) incorporated feedback from community advisory boards to promote cultural appropriateness for their intervention. 5. Provide your assessment of why this theory would or would not be a good fit for the program you are proposing for your Health Promotion Program Proposal The overarching factor that emerged from the Maxwell et al. (2014) study was that there is rarely a one-size-fits-all approach to developing the most efficacious interventions for different populations and a good fit for a specific program must be carefully created. The fact that these researchers invested significant amounts of time and effort in crafting the custom health behavior framework, including soliciting feedback from community advisory groups concerning the cultural appropriateness of their model indicates that this same approach would be useful for the envisioned health promotion program.

Healthcare Providers and Virus

infection prevention and control theory, critically discuss the challenges of managing Hepatitis in the community One of the key public health issues that impacts innumerable individuals worldwide is viral hepatitis. This virus leads to substantial human mortality and morbidity from severe infection as well as chronic sequelae (including cirrhosis and chronic active hepatitis (with regard to hepatitis , C & D). One among the ten commonest cancers that emerges across the globe -- hepatocellular carcinoma -- has been found to be linked closely to hepatitis as well as, in some areas across the globe, to hepatitis C (Zuckerman., 2003). HV or Hepatitis virus which belongs to the hepadna virus cluster is a double-stranded DNA virus that, atypically, gets reproduced via reverse transcription. HV is endemic among humans and even hyper-endemic in several areas across the globe. Researchers have delineated various variants of the HV virus. Natural infections by…...

mla Bibliography Beltrami, E., Williams, I., Shapiro, C., & Chamberland, M. (2000). Risk and Management of Blood-Borne Infections in Health Care Workers. Clin Microbiol Rev., 385 -- 407. Baumert TF, Blum HE. (2000). Hepatitis B virus mutations: molecular biology and clinical relevance. Vir Hep Rev.6:177 -- 192 Baumert TF, Barth H, Blum HE. (2005) Genetic variants of hepatitis B virus and their clinical relevance. Minerva Gastroenteroldietol. 51:95 -- 108. Baumert TF, Rogers SA, Hasegawa K, Liang TJ. (1996). Two core promotor mutations identified in a hepatitis B virus strain associated with fulminant hepatitis result in enhanced viral replication. J Clin Invest. 98:2268 -- 2276.

Immunization of Vaccine Hepatitis B Vaccine

Immunization Vaccine # 1 Name of Vaccine Rotavirus vaccine Trade Name RotaTeq® Type of vaccination Attenuated Contraindications · The previous dose of the Rotavirus vaccine was suspected of having a life-threatening allergic reaction. · Any component of the rotavirus vaccine was suspected of having a severe allergic effect. · Rotavirus vaccine was suspected of having Severe immunodeficiency (SCID). Precautions Anyone taking the Rotavirus vaccine should take several precautions, which include: pre-existing acute gastrointestinal conditions such as short gut syndrome or Hirschsprung’s disease and congenital malabsorption syndrome. Another precaution to take is chronic gastroenteritis. (Salvadori & Saux, 2010). Adverse Drug Reactions Some of the reactions that might be triggered by the vaccine include swelling on both throat and face, increased heartbeat, drowsiness, and breathing complications (CDC, 2019). Minimum Age to Receive Vaccine All Rotavirus vaccine doses should be given to children between 15 weeks and 8 months. (CDC, 2019). Routine Recommended Vaccine Schedule The dose should be initiated to children at 2nd ,4th, and 6th months. Minimum Interval Between Doses The recommended spacing…...

mla References Centers for Disease Control and Prevention. Routine vaccine recommendations. Retrieved from   Centers for Disease Control and Prevention. Special situations. Retrieved from https://www.cdc.gov/vaccines/ Mayo Clinic. (2020). Hepatitis B vaccine (Intramuscular route). Retrieved from  https://www.mayoclinic.org/  Otsuka-Ono, H., Hori, N., Ohta, H., Uemura, Y., & Kamibeppu, K. (2019). A childhood immunization education program for parents delivered during late pregnancy and one-month postpartum: a randomized controlled trial. BMC Health Services Research, 19. Retrieved from  https://bmchealthservres.biomedcentral.com/articles/10.1186/s12913-019-4622-z  Rogers, K. (2019). Immunization noncompliance: Gauging the cause, effect, and management in the school setting. NASN School Nurse, 34(3).  https://doi.org/10.1177/1942602X18799868  Salvadori, M., & Saux, N. (2010). Recommendations for the use of rotavirus vaccines in infants. Paediatr Child Health, 15(8), 519-523. DOI: 10.1093/pch/15.8.519. Sjogren, E., Ask, L., Ortqvist, A., & Asp, M. (2017). Parental conceptions of the rotavirus vaccine during implementation in Stockholm: A phenomenographic study. Journal of Child Health Care, 21(4).  https://doi.org/10.1177/1367493517734390  VAERS. (2020). Report an adverse event to VAERS. Retrieved from  https://vaers.hhs.gov/ https://www.cdc.gov/vaccines/vpd/rotavirus/hcp/recommendations.html 

Hepatitis of the Liver and How They

hepatitis of the liver and how they are transmitted to how we can find a remedy to slow down the deterioration process if not cure it completely. Hepatitis Hepatitis A Hepatitis B Causes of hepatitis B Transmission of hepatitis B Symptoms Tests for hepatitis B Self-protection Hepatitis C isk Factors for HCV Infection Consequences of HCV Infection Diagnosis Hepatitis is the disease connected with the inflammation of the liver. This disease was not discovered too long ago, however doctors and researchers have been able to find out the causes of hepatitis. There are several causes such as, viral, parasitic, infiltrative, drug or alcohol induced, or non-specific. Before a person is even diagnosed with this disease some of the prominent indications of the acute phase can be ranging from a symptomatic, where we may not even be able to notice we have hepatitis to feeling extremely tired, jaundice- where our skin or our eyes become yellow, nausea, vomiting, or even diarrhea. When the concerned…...

mla References A Commitment to Global Health - Text version, available at:   accessed on: http://www.niaid.nih.gov/director/usmed/1999/usmed99text.htm , February 9, 2004 BioE: News and Press Releases, available at: accessed on: February 9, 2004 http://www.bioe.com/news.html,

Hepatitis C

Hepatitis C: New CDC Screening Recommendations The objective of this study is to review the article written by Doug Campos-Outcalt entitled "Hepatitis C: New CDC Screening Recommendations" published in the Journal of Family Practice, Volume 61, Number 12 in December 2012. Campos-Outcalt (2012) writes that the Centers for Disease Control and Prevention (CDC) released new recommendations for Hepatitis C virus (HCV) infection screening including a one-time screening for all individuals in the United States that were born between the year of 1945 and 1965 "regardless of risk." The new recommendations are reported to be rather than a replacement to be instead an enhancement of "the recommendations for HCV screening" stated in 1998 calling for those who were considered high-risk to be screened. HCV results in a high level of morbidity and mortality in the United States. There are reported to be 17,000 new infections to have occurred in 2010 with approximately 2.7 to…...

mla It is reported that the two groups at the highest risk for HCV are those who are users of illegal drugs, which they injected, and those who received blood transfusions prior to 1992 when HCV blood screening began. There are other risk factors, which include having been incarcerated, having sex with someone infected with HCV, and the acquisition of a tattoo at an establishment that was unregulated, among others risk factors for contracting HCV. According to Campos-Outcalt, sustained virological response following treatment was demonstrated in individuals exhibiting a "reduction in all-cause mortality >50% compared with nonresponders." (Campos-Outcalt, 2012) Individuals born between 1988 and 1994 are much more likely to have contracted HCV than those born between 1999 and 2002. Observational Studies and Reported Outcomes Twelve observational studies are reported that examined treatment effects on the incidence of HCC and are reported to have shown a "75% reduction in HCC rates in those who achieved viral clearance compared with those who did not." (Campos-Outcalt, 2012) Physicians are advised that if there is a positive on a confirmatory test that the patient should be assumed to have HCV infection. The patient must decide if treatment is to be initiated and must undergo additional assessment to check for chronic liver disease. Measures should be taken to protect their liver from receiving additional damage including alcohol consumption reduction, medication avoidance and use of herbal products that result in liver damage. Patients infected with HCV should focus on the maintenance of an optimal weight and should receive vaccines against hepatitis A and B. AS well, patients should be instructed on how to avoid spreading the HCV infection to other people. There is noted by Campos-Outcalt (2012) to be controversies on HCV screening in regards to improvements in outcomes. For this reason the U.S. Preventive Services Task Force is presently conducting a revisement of the HCV recommendations for screening.

What are the essential immunizations needed for infants and children?

1. The Impact of Immunizations on Public Health 2. Debunking Myths About Immunizations 3. The History and Development of Vaccines 4. The Importance of Childhood Immunizations 5. Immunizations: Protecting Against Preventable Diseases 6. The Controversy Surrounding Immunizations 7. Immunizations: A Global Perspective 8. The Economics of Immunizations 9. Immunizations for Adults: Why They Are Important 10. The Future of Immunizations: Advances and Challenges 11. Common childhood vaccines include the measles, mumps, and rubella (MMR) vaccine, polio vaccine, hepatitis B vaccine, diphtheria, tetanus, and pertussis (DTaP) vaccine, varicella (chickenpox) vaccine, Haemophilus influenzae type b (Hib) vaccine, and the pneumococcal conjugate vaccine. These....

Essential Immunizations for Infants and Children Immunization plays a crucial role in protecting infants and children from a wide range of potentially life-threatening diseases. The recommended immunization schedule is based on the best available scientific evidence and is designed to provide optimal protection at different stages of development. Immunization Schedule The following is the recommended immunization schedule for infants and children in the United States, as outlined by the Centers for Disease Control and Prevention (CDC): 0-6 months: Hepatitis B (HepB) Rotavirus (RV) Diphtheria, Tetanus, and Pertussis (DTaP) Haemophilus influenzae type b (Hib) Pneumococcal conjugate (PCV13) 6-18 months: DTaP (2nd and 3rd doses) Hib (2nd....

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Essays About Hepatitis C

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Lovers and Livers by Jacalyn Duffin: a Look at The Dangers of The Hepatitis C Disease

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72 Hepatitis Essay Topic Ideas & Examples

🏆 best hepatitis topic ideas & essay examples, ⭐ good research topics about hepatitis, 📃 simple & easy hepatitis essay titles.

• Management of Hepatitis in the United Arab Emirates This directive was to affect the Ministry of Health of Dubai and Abu Dhabi and was to affect every new person with the intention of visiting the country.
• Management of Hepatitis B Virus Infection In the US, the cases of newly acquired hepatitis B virus infections have reduced significantly due to the success of public health management in the execution of an intensive national immunization policy.
• Hepatitis C: Prevention and Treatment PICOT Question: Compared to no screening, does obligatory screening for hepatitis C increase the timely diagnosis of the infection within 12 months in patients with immunity problems? The second study evaluates the effectiveness of screening […]
• A Hepatitis Incident in North Dakota However, a review of the news presented on the North Dakota Department of Health website showed that a hepatitis incident caused the most significant concern in the state over the studied period.
• “Investigating Acute Hepatitis…” Article by Prinzi Some major points that the author explains concern the primary causes of hepatitis, possible contributors, and the current state of the investigation regarding the outburst of the infection.
• Communicable Diseases: Hepatitis C The disease poses a threat to the public health of global populations and health security due to the increase in the number of international travel and the economic growth of countries.
• Disease Surveillance Program: Hepatitis A Awareness The disease’s ease of spread requires health organizations to formulate a disease surveillance program and communication plan to educate and empower the affected population to understand their role in upholding community wellness.
• Epidemiology of Hepatitis A in Australia In Australia, the prevalence rates of HAV among young children under the age of five in Queensland were 10 and 264 per 100 000 people in non-Indigenous and Indigenous populations respectively between 1999 and 2002.
• Chronic Hepatitis B in Chicago Area Analysis By analyzing the issue closer and identifying the factors causing the increase in the number of hepatitis B patients, one will be able to locate the means of addressing the problem.
• Hepatitis B & Jaundice: Diagnosis and Treatment 9 acute hepatitis B without delta-agent and without hepatic coma, 3) B18. 9 Acute hepatitis B without delta-agent and without hepatic coma.
• Hepatitis C and HIV Among Intravenous Drug Users In relation to this health issue of HIV and HCV, the community health nurse has the responsibility of promoting health among intravenous drug users.
• Hepatitis C: Causes, Risk Factors, and Treatment The major cause of Hepatitis C is the Hepatitis C virus. The blood test is capable of revealing the type of Hepatitis C an individual is suffering from, for instance, chronic Hepatitis C.
• Chronic Hepatitis B in Chicago The condition leads to the scarring of the organ. A liver biopsy can also be used to determine the extent of the problem.
• Diagnosis, Treatment and Prevention and Control Hepatitis A Serological tests to differentiate between hepatitis B and A were developed in the 1970’s and consequently led to the identification of the causative agents.
• Epidemiology of Hepatitis C in England The department of Public Health England estimates that 215,000 patients are infected with the chronic form of the disease in the United Kingdom; the prevalence of the infection in England is about 40 cases per […]
• Hepatitis A: Signs, Treatment, Prognosis The moment an individual is infected with this disease and the immune system has fought the hepatitis A virus successfully; this individual will never be infected again since his or her body is now permanently […]
• Clinical Virology Review: Hepatitis B Hepatitis B refers to inflammation in the liver while Hepatitis B virus is the important cause of Hepatitis. Acute and chronic Hepatitis B is a major health concern and is capable of leading to complications […]
• Hepatitis C: Data and Statistics for Chronic and Acute Types Hepatitis C is supposed to be the most common disease caused by a virus and transmitted by blood in the United States.
• Hepatitis A: A Fatal Infectious Disease That Affects the Liver Water is the medium of survival of the virus. The virus enters the body through the anal opening or the mouth.
• Transmittable Liver Infection, Known as the Hepatitis a Virus The causative agent is one of the different forms of hepatitis viruses that trigger inflammation and affect the proper functioning of the liver.
• Psycho-Social Aspects of Hepatitis C The gap in time between identifying the cause of a disease like hepatitis C and finding a way to prevent, control, or eradicate it is often, unfortunately, a long one.
• Genetically Modified Potato as Hepatitis B Vaccine The thesis presented here is an argument in favor of using genetically modified potatoes in the effective prevention of the deadly hepatitis B virus infection.
• Hepatitis C: Diagnosis and Treatment The diagnosis of chronic hepatitis C is made by history, serological testing and liver biopsy. The next drug available for the treatment of chronic hepatitis C is peginterferon-alpha.
• Hepatitis C: Clinical Research and New Treatments Genotyping is a significant development since it helps to determine the treatment regiment to be offered to the patient. Optimal tests for HCV infection have been developed, leading to the early diagnosis and treatment of […]
• Implications of Hepatitis C Virus Infection The paper offers the analysis of the research methodology, variables, and the study design. The hypothesis of the study has been that HCV influences the central nervous system “in a subset of infected individuals”.
• Hepatitis A, B, and C: Control and Management The term “Hepatitis” refers to a group of medical conditions characterized by inflammation of the liver cells hepatocytes, the basic units of the liver.
• Anticipating New Regimens with Direct Acting Antivirals for Hepatitis C The article written by Rena Fox is aimed at informing the audience about the approval of two drugs that can be used for the treatment of hepatitis C.
• Countering to the Hepatitis Disease The state of affairs is worsened by the limited fiscal resources allotted by the exchequer. It is noted that others are known to cut off sections of the clitoris.
• Prevalence of Hepatitis B Hence, it means that the high prevalence of hepatitis B in Sub-Saharan countries is attributable to childhood infections of HBV. High prevalence of hepatitis B in Sub-Saharan countries is due to numerous factors that promote […]
• Pathogenicity and Molecular Typing of Fowl Adenovirus-Associated With Hepatitis/Hydropericardium Syndrome in Central China
• History, Symptoms, and Treatment of Hepatitis C
• Interferon-α-Enhanced CD100/Plexin-B1/B2 Interactions Promote Natural Killer Cell Functions in Patients With Chronic Hepatitis C Virus Infection
• Educating About the Risks of Hepatitis B
• Hepatocyte Endoplasmic Reticulum Stress Inhibits Hepatitis B Virus Secretion and Delays Intracellular Hepatitis B Virus Clearance After Entecavir Treatment
• Identifying the Links Between HIV, Hepatitis, and Substance Misuse
• Hepatitis C-Associated Mixed Cryoglobulinemic Vasculitis Induces Differential Gene Expression in Peripheral Mononuclear Cells
• Hepatitis A,B,C,D,E,G: History, Symptoms, Causes, Treatment
• Mathematical Modeling for Hepatitis B Virus: Would Spatial Effects Play a Role and How to Model It?
• Autoimmune Hepatitis: Tolerogenic Immunological State During Pregnancy and Immune Escape in Post-partum
• Novel Immunotherapies for Autoimmune Hepatitis
• Edible Plant-Derived Vaccines Against Hepatitis B Virus
• Antibody Level After Hepatitis B Vaccination in Hemodialysis
• Cytoplasm-Translocated ku70/80 Complex Sensing of HBV DNA Induces Hepatitis-Associated Chemokine Secretion
• Natural Killer Cell Functional Dichotomy: A Feature of Chronic Viral Hepatitis?
• Treatment Methods for Patients Diagnosed With Hepatitis C Virus
• Preclinical Development and Production of Virus-Like Particles as Vaccine Candidates for Hepatitis C
• Developing Culturally Sensitive Interventions for Hepatitis B
• Patients With Chronic Hepatitis C Virus Infection Are at an Increased Risk of Colorectal Cancer: A Nationwide Population-Based Case-Control Study in Taiwan
• Hepatitis and the Impact of the Disease on Emergency Medical Workers
• Interaction and Mutual Activation of Different Innate Immune Cells to Kill and Clear Hepatitis C Virus-Infected Cells
• Blood and Bio Identity: Ideas About Self, Boundaries, and Risk Among Blood Donors and People Living With Hepatitis C
• Plant Extracts From Cameroonian Medicinal Plants Strongly Inhibit Hepatitis C Virus Infection in Vitro
• Environmental Stability and Infectivity of Hepatitis C Virus In Different Human Body Fluids
• Glycan Shielding and Modulation of Hepatitis C Virus Neutralizing Antibodies
• Genetic Modified Potatoes Vaccines Based for Hepatitis B
• Psychosocial and Neurocognitive Factors Associated With Hepatitis C Implications for Future Health and Wellbeing
• Relationship Between Schistosomiasis and Hepatitis C
• Characteristics and Specialist Linkage to Care of Patients Diagnosed With Chronic Hepatitis C Across Different Settings in an Urban Academic Hospital: Implications for Improving Diagnosis and Linkage to Care
• Advanced Glycation End Products as a Predictor of Diabetes Mellitus in Chronic Hepatitis C-Related Cirrhosis
• Living With Hepatitis C’s Stigma of Getting Infected While Doing Bad Things
• Transmission, Diagnosis, and Treatment of Hepatitis B
• Knowledge, Attitudes, and Behaviors of Viral Hepatitis Among Recent African Immigrants in the United States: A Community Based Participatory Research Qualitative Study
• Aspirin Use and the Incidence of Hepatocellular Carcinoma in Patients With Hepatitis B Virus or Hepatitis C Virus Infection
• Hepatitis Types and Ems Implications
• Links Between Human Line-1 Retrotransposons and Hepatitis Virus-Related Hepatocellular Carcinoma
• Immune Status Against Hepatitis B in Patients After Allogeneic Hematopoietic Cell Transplantationfactors Affecting Early and Long-Lasting Maintenance of Protective Anti-hbs Titers
• Hepatitis B Vaccine for Newborns, Why It’s Important
• Molecular Biology and Infection of Hepatitis E Virus
• Low Mannose Binding Lectin, but Not L-Ficolin, Is Associated With Spontaneous Clearance of Hepatitis C Virus After Infection
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IvyPanda. (2024, February 28). 72 Hepatitis Essay Topic Ideas & Examples. https://ivypanda.com/essays/topic/hepatitis-essay-topics/

"72 Hepatitis Essay Topic Ideas & Examples." IvyPanda , 28 Feb. 2024, ivypanda.com/essays/topic/hepatitis-essay-topics/.

IvyPanda . (2024) '72 Hepatitis Essay Topic Ideas & Examples'. 28 February.

IvyPanda . 2024. "72 Hepatitis Essay Topic Ideas & Examples." February 28, 2024. https://ivypanda.com/essays/topic/hepatitis-essay-topics/.

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IvyPanda . "72 Hepatitis Essay Topic Ideas & Examples." February 28, 2024. https://ivypanda.com/essays/topic/hepatitis-essay-topics/.

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