Analytical Essay on Hepatitis B and Hepatitis C: Pathophysiology and Clinical Presentation, Infection Prevention and Control Considerations

NB: We do not resell your papers. Upon ordering, we do an original paper exclusively for you.

NB: All your data is kept safe from the public.

Introduction

Hepatitis B and hepatitis C are highly infectious diseases and occur due to being infected by the hepatitis B virus (HBV) and the hepatitis C virus (HCV) respectively. Millions of people worldwide are infected with these viruses and the infected population can suffer from long term complications such as liver cirrhosis or hepatocellular carcinomas (Busch & Thimme, 2015). A contrast and comparison of both HBV and HCV will be presented in this report. The viruses’ morphology, epidemiological features, pathophysiology, clinical presentation and immune system responses will be examined and measured. Legislative requirements will also be highlighted alongside infection prevention and control measures.

Etiology, Morphology, Incidence and Prevalence

The HBV antigen, originally named the Australia antigen, was first recognised in 1967 by Dr Blumberg (Saeed, Waheed, & Ashraf, 2014). This virus spreads through mucosal and percutaneous exposure to infected blood or other bodily fluids, including salvia, seminal, and vaginal fluids. Infection can also occur through perinatal, and horizontal transmission (Hyun, Lee, Ventura, & McMenamin, 2017; Orlando et al., 2015). Similarly, HCV is likewise transmitted through percutaneous blood exposure. This exposure is generally a result of unsafe intravenous drug administration, perinatal exposure, high risk sexual activity, use of unsterilized medical equipment and administration of blood products not tested for HCV (Manns et al., 2017).

HBV is a double-stranded Deoxyribonucleic acid (DNA) virus and is a part of the hepadnaviruses family, while the HCV is a single stranded spherical ribonucleic acid (RNA) virus from the Flavivirus family. The HBV virion, commonly known as the Dane particle, is a double shelled particle. The outer envelope encloses the surface antigen known as the (HBsAg), while the inner envelope contains the viral nucleocapsid element of HBV core antigen (HBcAg). It is the HBcAg-derived peptides which stimulate the infected person’s cellular immune response against HBV (Doo & Ghany, 2010; World Health Organization, 2015). HCV is an enveloped virus that has an inner core of RNA which is encased in a protective protein shell, which is surrounded by a lipid envelope (Dubuisson & Cosset, 2014). Embedded within the lipid envelope are E2 and E1, which are glycoproteins required for the virus to viral attachment and cellular fusion (Dubuisson & Cosset, 2014; Freedman, Logan, Law, & Houghton, 2016). It is the HCV core protein that is a key factor in the development of liver disease; it affects the cell cycle regulation, cell growth promotion, cell proliferation, lipid metabolism and apoptosis (Mahmoudvand, Shokri, Taherkhani, & Farshadpour, 2019). There are seven different HCV genotypes, and they are classified accordingly (1-7). Genotype 1 being the most common. Genome 1 accounts for 46.2 percent of cases of HCV (Mohamed, 2015).

A systematic review performed by Ott, Stevens, Groeger & Wiersma (2012) reviewed the prevalence of HBsAg globally over a 27-year period. From their review, it was determined that the global prevalence of HBV in 2005 was 3.7 percent, with an estimated 240 million people infected. The region with the highest HBV incidence was the western sub-saharan of Africa. (Ott et al., 2012). HBV has an estimated 786,000 deaths each year (Lozano et al., 2012). A report by Petruzziello, Marigliano, Loquercio, Cozzolino & Cacciapuoti (2016) showed that the worldwide prevalence of HCV infection was an estimated 177.5 million people. HBV is more commonly reported in developing countries in Asia and Africa, with lower prevalence rates in industrial nations (Mohamed, 2015). HCV has been considered one of the world’s leading causes of morbidity and mortality, however overall HBV has a higher incidence.

Pathophysiology and Clinical Presentation

The HBV has an incubation period of 12 weeks on average, this is the acute infection phase (Baker, 2017). During the acute infection phase, clinical manifestations include fatigue, jaundice, vomiting, nausea, and pain (abdominal, arthralgia, and myalgia) (Busch & Thimme, 2015). Between 60 and 95 percent of infected individuals are asymptomatic (Mantzoukis et al., 2017). However, the clinical manifestations cannot distinguish an acute HBV infection from the other forms of acute viral hepatitis (Busch & Thimme, 2015). The constantly proliferating hepatocytes cause the virus to continue to shed into the blood stream, this contributes to the acute infection developing into a chronic HBV infection (McMahon, 2008). This signifies that the immune system has been unsuccessful at eradicating the virus. HBV infection becomes chronic in five to ten percent of adults (Zuckerman & Zuckerman, 2010). Spontaneous conversion to HBsAG negativity occurs in roughly one to two per cent of chronic carriers, however in 20 percent of HBsAG-positive carriers’ spontaneous reactivation of HBV occurs (Torresi, 2010). Chronic HBV infection can have long term complications, this includes cirrhosis, liver fibrosis, and hepatocellular carcinoma (Baker, 2017). 80 percent of all hepatocellular carcinomas are a result of chronic HBV (Torresi, 2010).

The initial period where a person becomes infected with HCV is known as an acute infection. This incubation period lasts 15 to 150 days, with people mainly presenting with fatigue, weakness, or malaise (Westbrook & Dusheiko, 2014). During this period the infection can be cleared spontaneously by the host immune system, through cell medicated response (Terilli & Cox, 2012). However, 75 to 85 percent of patients fail to clear the disease, and if the HCV virus remains for more than six months it is considered a chronic HCV infection, and progressive liver damage is likely to occur (Cobo, 2014). The development of liver cirrhosis and further hepatic complications occurs in 15 to 30 percent of patients with chronic hepatitis C, and this occurs over the course of 20 to 30 years (Centre of Disease Control and Prevention, 2018). This progression is hypothesised to occur due to locally driven immune responses, which can lead to hepatic decompensation with clinical manifestations such as upper gastrointestinal bleeding, ascites, hepatic encephalopathy. Further progression can result in the development of hepatocellular carcinoma (Ismail & Cabrera, 2013).

The Role of the Immune System

The immune system is critical in HBV and HCV infections for determining the outcome of the infection. Innate and adaptive immunity is the first line of defence to protect the body against the virus, as it provides recognition of viral proteins and fights the production of interferons (Tan, Koh, & Bertoletti, 2015). Activation of acquired immunity is an essential component of adaptive responses, this is through the production of antigens and their specific responses.

The innate immune response has a weak activation in HBV infections, this is a result of a lack of induction of interferons α and β (Tan et al., 2015). This is hypothesised to be caused by the HBV escaping innate recognition, and inhibiting the virus’s replication (Chisari, Isogawa, & Wieland, 2010). In an acute infection, the adaptive immune responses have been recognised as important in the resolution of the HBV. This response includes different effector cell types including Cluster of Differentiation (CD) 4 T cells and CD8 cytotoxic T lymphocytes and B cell antibody production (Tan et al., 2015). These are required to eradicate HBV infected hepatocytes by noncytokine and cytokine mechanisms, and therefore they can reduce the overall circulating viral levels (Cheng et al., 2017). It is the B cell antibody production which assists in preventing reinfection by neutralising free viral particles. The adaptive anti-viral immune response is only induced after an acute infection has occurred. The CD8 T-cell responses are important in an acute infection but cannot clear the virus in chronic carriers (Chisari et al., 2010; Mackie, 2011). It is these processes that cause alanine aminotransferase (ALT) to be released and can result in the development of cirrhosis due to the production of liver fibrosis (Trépo, Chan, & Lok, 2014). This immune response being so vigorous and aggressive can be the cause for such a fulminant HB infection, and therefore improving antiviral immunity can assist in controlling the HBV (Tan et al., 2015; Trépo et al., 2014)

Similar to HBV, the innate and adaptive immune responses are a key factor in the viral clearance of HCV, however these responses are often mild and facilitate the development of chronic infection but can prevent liver damage (Manns et al., 2017; Spengler, Nischalke, Natterman, & Strassburg, 2013). Natural killer cells are considered to be involved in the innate immune response to clear the HCV infection (Dustin, 2017). The adaptive immune response, similar to HBV, relies on T cell and antibody responses to control the infection. However, these antibodies have been shown to have limited activity against the HCV (Dustin, 2017). Comparable to HBV, spontaneous viral clearance is a consequence of CD4 and CD8 T cell responses. The HCV maintains persistent and this has been attributed to early loss of or inadequate T cell responsiveness (Spengler et al., 2013). Interferon stimulating genes are produced during the acute phase of HCV, but similarly to HBV this causes a poor response, and is ineffective at clearing the virus (Dustin, 2017). Chronic HCV infection evolves most commonly due to an alteration of immune responses or rapid exhaustion. The effect of immune system is apparent in the clearance of HBV and HCV; these responses are both positive and negative shows that there is the possibility of development to become a chronic carriage with liver protection mechanisms. However, more research is required to fully understand the immune response in all viral hepatitis diseases.

Diagnosis

Australian health professionals need to follow the National Hepatitis B Testing Policy when diagnosing HB (National Hepatitis B Virus (HBV) Testing Policy Expert Reference Committee, 2015). This policy helps guide health professionals and insures that current testing practices are upheld. As previously mentioned, the HBV is impossible to differentiate from other hepatitis viruses, and therefore proper laboratory diagnosis is critical for confirmation of the disease (World Health Organisation, 2018a). There are multiple tests that can diagnose and monitor people infected with HBV and can distinguish between an acute or chronic infection (World Health Organisation, 2018a). Tests to detect HBsAg and HBeA called serologic protein antigen tests, and antiHBs, anti-HBe, IgM anti-HBc, and total anti-HBC, are detected through serologic antibody assays (Baker, 2017). These tests can determine if a person has a HBV infection, if it is acute or chronic, how long they may have had the infection, what phase of chronic infection they are in, if a person has cleared the infection, or is immunised against the HBV (Hepatitis Victoria, 2019). Other tests such as the polymerase chain reaction assay, and nucleic acid amplification testing are recommended by Baker (2017) within the “Red Book” and they can detect and enumerate HBV DNA in serum or plasma. However, this is from an American text and some of these tests are not frequently used in Australia for just a diagnosis of HBV, but more so for reference testing.

HCV is commonly asymptomatic, and therefore diagnostic testing is rarely done during an acute infection phase and are mostly performed on people who have developed a chronic HCV infection, but usually only once secondary conditions develop (World Health Organisation, 2018b). Currently in Australia a person is first screened for HCV through a serology test also known as an antibody test, this test indicates if the person has had exposure to HCV, this can either be a past or current infection (Burke, 2014). The method for confirmation of diagnosis for a current HCV infection is through a polymerase chain reaction assay to look for HCV RNA. This test can indicate the presence of the HCV virus, and the viral load. As a result, this test is important to perform as a person with a positive serology test can be positive for multiple repeated serology tests but has no detectable HCV RNA in the assay (Holmes, Thompson, & Bell, 2013). This can be a result of a past HCV infection which has spontaneously cleared or been cleared through treatment. The National Hepatitis C Testing Policy released by the Australian Government Department of Health recommends that a person be subjected to at least two serology tests if deemed reactive before being subjected to supplemental testing to confirm a true positive result (National Hepatitis B Virus (HBV) Testing Policy Expert Reference Committee, 2015). Once a true positive result is confirmed, further testing should be done to determine the degree of liver damage as a result of the HCV infection. This should include a liver functioning profile, liver imaging, and/or liver biopsy (Holmes et al., 2013).

Infection Prevention and Control Considerations

HBV and HCV infections are considered to be a principal public health concern, this is due to its commonality, long lasting health impact, and that infected persons are often unaware that they have the infectious disease (Centres for Disease Control and Prevention, 2019). People who identify as indigenous Australians, people who participate in high risk sexual activity, and intravenous drug users are considered the be at high risk of being infected with HBV (Communicable Diseases Network Australia (CDNA), 2018). Likewise, HCV is most prevalent in intravenous drug users, but also through unsterile medical procedures such as blood transfusions, or unsterile vaccinations, this is more common in developing countries (Holmes, Thompson, & Bell, 2013). Therefore, education to the general public and health professionals is essential to reduce prevalence, and also ensure early diagnosis to ameliorate overall outcomes (Ditah et al., 2014).

As mentioned, intravenous drug users are at the most risk from transmission of HBC and HCV, thus implementing safe infection sites with medical supervision has been shown to reduce the risk of blood borne infections in intravenous drug users (Gastroenterological Society of Australia, 2018). These sites aid in providing sterile needles, reducing needle sharing, and by providing education on harm minimisation strategies.

Within a health care setting the prevention and control of HBV and HCV infections revolves around adherence to standard precautions (Gastroenterological Society of Australia, 2018). Through standard precautions health professionals treat all patients with the assumption that their body fluid or blood is potentially infectious. Isolation of patients with either virus is not required (Gastroenterological Society of Australia, 2018). However, ensuring that all health care workers and at-risk individuals are vaccinated against HBV is paramount in reducing the potential for the infection to spread. As health care workers can be more exposed to the HBV and HCV infected population, as well as other blood borne infectious diseases education of safe needle handling and phlebotomy is critical to reduce the prevalence of needle stick injuries, which can result in the health care worker seroconversion depending on if it is a HBV or HCV infection, and the viral proteins present, can be of low to high risk (Holmes et al., 2013).

Within areas of high prevalence of hepatitis b and c, including correctional facilities and haemodialysis units, increased screening has been identified has a way to control the infection risk, and provide early treat treatment for patients, while also minimising the risk to the overall population in these areas (MacArthur et al., 2014).

Legislative reporting requirements and Drug Resistance

Within Australia both HBV and HCV are notifiable diseases in every state and territory. Specifically, in Victoria, there is a statutory requirement where notification to the Department of Health, in writing, is required within five days of a diagnosis of hepatitis b or c. This is under the under the Public Health and Wellbeing Regulations 2009 (Communicable Diseases Network Australia (CDNA), 2018).

For a patient receiving treatment for hepatitis b or c one way is through antiviral medication. The main aim for antivirals is to reduce the virus from replicating and further damaging the liver, thereby making it possible for the liver to somewhat repair its self, but it is unlikely to provide much in the way of a cure (Kim, Han, & Ahn, 2016). However, these antivirals can cause the HBV to mutate, causing the antivirals to become less effective at targeting the HBV (Keeffe et al., 2006). This drug resistance is a nationwide concern, as more and more viruses and bacterium are mutating and causing our current forms of treatment to become redundant (Kim et al., 2016). Therefore, it is important for the patient to be closely monitored during treatment to monitor for signs of resistance.

Conclusion

In conclusion, an overview and comparison of HBV and HCV was delivered in this report with focus on the viruses’ morphology, epidemiology, aetiology, clinical presentations, pathophysiology, diagnosis, immune response, and implications for infection prevention and control, and legislative requirements. Overall, it shows that it is prevention, early diagnosis, monitoring, and early treatment which are pivotal in reducing the incidence, long term complications, and recognising resistance to treatment.

References

Baker, C. (2017). Red book. Elk Grove Village, IL: American Academy of Pediatrics.
Burke, M. (2014). HIV, viral hepatitis & STIs. Melbourne: Australasian Society for HIV Medicine (ASHM).
Busch, K., & Thimme, R. (2015). Natural history of chronic hepatitis B virus infection. Medical Microbiology and Immunology, 204(1), 5-10. doi:10.1007/s00430-014-0369-7
Centre of Disease Control and Prevention. (2018). Hepatitis C Questions and Answers for the Public | CDC. Retrieved from https://www.cdc.gov/hepatitis/hcv/cfaq.htm
Centres for Disease Control and Prevention. (2019). What is Viral Hepatitis? | Division of Viral Hepatitis | CDC. Retrieved from https://www.cdc.gov/hepatitis/abc/index.htm
Cheng, X., Xia, Y., Serti, E., Block, P. D., Chung, M., Chayama, K., … & Liang, T. J. (2017). Hepatitis B virus evades innate immunity of hepatocytes but activates cytokine production by macrophages. Hepatology, 66(6), 1779-1793.
Chisari, F. V., Isogawa, M., & Wieland, S. F. (2010). Pathogenesis of hepatitis B virus infection. Pathologie Biologie, 58(4), 258-266. doi:http://dx.doi.org/10.1016/j.patbio.2009.11.001
Cobo, F. (2014). Viral hepatitis. Imported Infectious Diseases, 213-225. doi: 10.1533/9781908818737.213
Communicable Diseases Network Australia (CDNA). (2018). Hepatitis B – CDNA National Guidelines for Public Health Units. Canberra: CDNA.
Ditah, I., Ditah, F., Devaki, P., Ewelukwa, O., Ditah, C., Njei, B., . . . Charlton, M. (2014). The changing epidemiology of hepatitis C virus infection in the United States: National health and nutrition examination survey 2001 through 2010. Journal of Hepatology, 60(4), 691-698. doi:http://dx.doi.org/10.1016/j.jhep.2013.11.014
Doo, E., & Ghany, M. (2010). Hepatitis B Virology for Clinicians. Clinics in Liver Disease, 14(3), 397-408. doi: 10.1016/j.cld.2010.05.001
Dubuisson, J., & Cosset, F. (2014). Virology and cell biology of the hepatitis C virus life cycle – An update. Journal of Hepatology, 61(1), S3-S13. doi: 10.1016/j.jhep.2014.06.031
Dustin, L. (2017). Innate and Adaptive Immune Responses in Chronic HCV Infection. Current Drug Targets, 18(7), 826-843. doi: 10.2174/1389450116666150825110532
Freedman, H., Logan, M., Law, J., & Houghton, M. (2016). Structure and Function of the Hepatitis C Virus Envelope Glycoproteins E1 and E2: Antiviral and Vaccine Targets. ACS Infectious Diseases, 2(11), 749-762. doi: 10.1021/acsinfecdis.6b00110
Gastroenterological Society of Australia. (2018). Australian recommendations for the management of hepatitis C virus infection: a consensus statement (September 2018). Melbourne: Gastroenterological Society of Australia.
Hepatitis Victoria. (2019). Hepatitis B Testing. Retrieved from https://www.hepvic.org.au/page/7/hepatitis-b-testing
Holmes, J., Thompson, A., & Bell, S. (2013). Hepatitis C An update. Australian Family Physician, 42, 452-456. Retrieved from http://www.racgp.org.au/afp/2013/july/hepatitis-c/.
Hyun, S., Lee, S., Ventura, W., & McMenamin, J. (2017). Knowledge, Awareness, and Prevention of Hepatitis B Virus Infection Among Korean American Parents. Journal of Immigrant And Minority Health, 20(4), 943-950. doi: 10.1007/s10903-017-0609-1
Ismail, B. E. S., & Cabrera, R. (2013). Management of liver cirrhosis in patients with hepatocellular carcinoma. Chinese clinical oncology, 2(4).
Keeffe, E. B., Dieterich, D. T., Han, S. H. B., Jacobson, I. M., Martin, P., Schiff, E. R., … & Wright, T. L. (2006). A treatment algorithm for the management of chronic hepatitis B virus infection in the United States: an update. Clinical Gastroenterology and Hepatology, 4(8), 936-962.
Kim, S., Han, K., & Ahn, S. (2016). Hepatitis C Virus and Antiviral Drug Resistance. Gut and Liver, 10(6), 890-895. doi: 10.5009/gnl15573
Lozano, R., Naghavi, M., Foreman, K., Lim, S., Shibuya, K., Aboyans, V., … & AlMazroa, M. A. (2012). Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010. The lancet, 380(9859), 2095-2128.
MacArthur, G. J., van Velzen, E., Palmateer, N., Kimber, J., Pharris, A., Hope, V., . . . Hutchinson, S. J. (2014). Interventions to prevent HIV and Hepatitis C in people who inject drugs: A review of reviews to assess evidence of effectiveness. International Journal of Drug Policy, 25(1), 34-52. doi:http://dx.doi.org/10.1016/j.drugpo.2013.07.001
Mackie, P. (2011). Major virus groups. In T. Elliott, A. Casey, P. Lambert, & J. Sandoe (Eds.), Medical Microbiology and Infection. Chichester: Wiley-Blackwell.
Mahmoudvand, S., Shokri, S., Taherkhani, R., & Farshadpour, F. (2019). Hepatitis C virus core protein modulates several signaling pathways involved in hepatocellular carcinoma. World Journal of Gastroenterology, 25(1), 42-58. doi: 10.3748/wjg.v25.i1.42
Manns, M., Buti, M., Gane, E., Pawlotsky, J., Razavi, H., Terrault, N., & Younossi, Z. (2017). Hepatitis C virus infection. Nature Reviews Disease Primers, 3, 17006. doi: 10.1038/nrdp.2017.6
Mantzoukis, K., Rodríguez-Perálvarez, M., Buzzetti, E., Thorburn, D., Davidson, B., Tsochatzis, E., & Gurusamy, K. (2017). Pharmacological interventions for acute hepatitis B infection. Cochrane Database of Systematic Reviews. doi: 10.1002/14651858.cd011645.pub2
McMahon, B. J. (2008). Natural history of chronic hepatitis B–clinical implications. The Medscape Journal of Medicine, 10(4), 91.
Mohamed, A. (2015). Hepatitis C virus: A global view. World Journal of Hepatology, 7(26), 2676. doi: 10.4254/wjh.v7.i26.2676
National Hepatitis B Virus (HBV) Testing Policy Expert Reference Committee. (2015). National Hepatitis B Testing Policy v1.2. Canberra: Australian Government Department of Health.
Orlando, R., Foggia, M., Maraolo, A., Mascolo, S., Palmiero, G., Tambaro, O., & Tosone, G. (2015). Prevention of hepatitis B virus infection: from the past to the future. European Journal of Clinical Microbiology & Infectious Diseases, 34(6), 1059-1070. doi: 10.1007/s10096-015-2341-x
Ott, J., Stevens, G., Groeger, J., & Wiersma, S. (2012). Global epidemiology of hepatitis B virus infection: New estimates of age-specific HBsAg seroprevalence and endemicity. Vaccine, 30(12), 2212-2219. doi: 10.1016/j.vaccine.2011.12.116
Petruzziello, A., Marigliano, S., Loquercio, G., Cozzolino, A., & Cacciapuoti, C. (2016). Global epidemiology of hepatitis C virus infection: An up-date of the distribution and circulation of hepatitis C virus genotypes. World Journal Of Gastroenterology, 22(34), 7824. doi: 10.3748/wjg.v22.i34.7824
Saeed, U., Waheed, Y., & Ashraf, M. (2014). Hepatitis B and hepatitis C viruses: a review of viral genomes, viral induced host immune responses, genotypic distributions and worldwide epidemiology. Asian Pacific Journal Of Tropical Disease, 4(2), 88-96. doi: 10.1016/s2222-1808(14)60322-4
Spengler, U., Nischalke, H., Natterman, J., & Strassburg, C. (2013). Between Scylla and Charybdis: the role of the human immune system in the pathogenesis of hepatitis C. World Journal of Gastroenterology, 19(44), 7852-7866.
Tan, A., Koh, S., & Bertoletti, A. (2015). Immune Response in Hepatitis B Virus Infection. Cold Spring Harbor Perspectives in Medicine, 5(8), a021428. doi: 10.1101/cshperspect.a021428
Terilli, R., & Cox, A. (2012). Immunity and Hepatitis C: A Review. Current HIV/AIDS Reports, 10(1), 51-58. doi: 10.1007/s11904-012-0146-4
Torresi, J. (2010). Hepatitis. In A. Yung, D. Spelman, A. Street, J. McCormack, T. Sorrell, & P. Johnson (Eds.), Infectious diseases: A clinical approach (3rd ed.). Melbourne: IP Communications.
Trépo, C., Chan, H. L. Y., & Lok, A. (2014). Hepatitis B virus infection. The Lancet, 384(9959), 2053-2063.
Westbrook, R., & Dusheiko, G. (2014). Natural history of hepatitis C. Journal Of Hepatology, 61(1), S58-S68. doi: 10.1016/j.jhep.2014.07.012
World Health Organisation. (2018a). Hepatitis B. Retrieved from https://www.who.int/news-room/fact-sheets/detail/hepatitis-b
World Health Organisation. (2018b). Hepatitis C. Retrieved from https://www.who.int/news-room/fact-sheets/detail/hepatitis-c
World Health Organization. (2015). Guidelines for the prevention, care and treatment of persons with chronic hepatitis B infection. Geneva, Switzerland: World Health Organization.
Zuckerman, J. N., & Zuckerman, A. J. (2010). Hepatitis viruses. In J. Cohen, W. Powderly, & S. Opal (Eds.), Infectious Diseases (3rd ed., Vol. Two, pp. 1539-1549). London: Mosby Elsevier.

Click Here To Order Now!