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Hepatitis

Kerri Alldis. Hepatitis Essay. October 2003.

Hepatitis is a virus. Viruses are small infectious agents that reproduce only in living cells. They are obligate intracellular parasites, depending on the host cell for small molecules, energy and synthesis of macromolecules (especially synthesis of proteins). Viruses cannot replicate apart from living cells. Viruses are among the smallest infectious agents and much smaller than the cells they infect. Viruses consist of a nucleic acid core surrounded by a protein shell. A membrane envelope may also be present. Viruses are a major cause of human disease (Madigan. et al., 2000).

Hepatitis is a systemic disease primarily involving the liver (Brooks et al., 2001). There are six known hepatitis viruses. These are types A, B, C, D, E and G. Hepatitis A virus (HAV) is a picornavirus. It is a spherical particle that contains a linear single-stranded RNA genome. Infectious hepatitis A is a virus-mediated inflammation of the liver, which is transmitted mainly by faecal contamination of water, food or milk (Madigan. et al., 2000). Hepatitis B virus (HBV) is a hepadnavirus that establishes chronic infections and is a major factor in the eventual development of liver disease and hepatocellular carcinoma. The viral genome consists of partially double stranded circular DNA. The HBV genome has four genes - pol, env, precore and X that respectively encode the viral DNA polymerase, envelope protein, precore protein and protein X (Worman, H.J., 1999).Hepatitis C virus (HCV) is a positive stranded RNA virus, classified as family Flaviviridae. The genome encodes a core protein, 2 envelope glycoproteins and several non-structural proteins (Brooks et al., 2001). Hepatitis D virus (HDV) is referred to as Delta Hepatitis. Hepatitis E virus (HEV) is a single stranded RNA virus that occurs in endemic form in developing countries where water supplies are sometimes faecally contaminated. Hepatitis G virus (HGV) has recently been discovered to be a member of the Flaviviridae family (Jawetz et al., 2001).

The hepatitis viruses are not directly cytopathic to the liver. The infected hosts immune response is responsible for the liver damage while trying to eradicate the virus from the liver. HAV and HEV are spread faecally-orally and are characterised by acute, self-limiting illness. Hepatitis B, C, and D viruses are usually spread by the blood. Hepatitis C infection often results in persistent replication. For hepatitis B infection, the final outcome is dependant upon the age of infection and the state of the host’s immune response (Locarnini, S., 2000). Following primary HCV infection, in most cases, persistent viraemia and chronic hepatitis develop (Freeman, A.J. et al., 2001).

The most common hepatitis viruses are forms A, B, and C. HBV causes chronic and acute infection. Acute hepatitis B can range from sub-clinical disease to fulminant hepatic failure. Many acutely infected individuals develop clinically apparent acute hepatitis with loss of appetite, nausea, vomiting, fever, abdominal pain and jaundice (Worman, H.J., 1999). About 80% of all acutely infected HCV individuals become chronically infected in which the virus is possibly never cleared (Worman, H.J., 1999).

HAV infection can be sub-clinical in mild cases or can lead to severe liver damage in chronic infections. The A type virus spreads from the intestine to the liver via the bloodstream and usually results in jaundice (Madigan. et al., 2000). Liver biopsy permits a tissue diagnosis of hepatitis. Serological tests are also used. The diagnosis of HBV infection is generally made on the basis of serology, as all infected individuals will have detectable serum hepatitis B surface antigen. Liver biopsy confirms the diagnosis (Worman, H.J., 1999).

There are marked differences in the epidemiological features of hepatitis A, B, and C infections. Hepatitis A virus is widespread throughout the world. Outbreaks are common in families, institutions and military groups. The most likely mode of transmission is via the faecal-oral route through close personal contact. Hepatitis A infection can occur at an early age u8nder crowded conditions and poor sanitation (Brooks et al., 2001). The most significant food vehicles for type A hepatitis are shellfish from waters that are polluted with human faeces but these will not cause infection if the food is cooked properly because heating destroys the virus (Madigan. et al., 2000).

HBV is in worldwide distribution. It is relatively rare in the United States but is endemic in parts of Asia. It is transmitted in the blood. The blood supply in developed countries has been screened form any years. Major routes of transmission in Western Countries are intravenous drug use and sexual contact (Worman, H.J., 1999).

Infections with HCV are extensive throughout the world and are transmitted by the blood (Brooks et al., 2001). High prevalence areas include South America and Asia. HDV is found throughout the world with a non-uniform distribution. The highest prevalence is in Italy and The Middle East. HDV infects all age groups but those at high risk are intravenous drug users and those who have had multiple blood transfusions (Jawetz et al., 2001).

Treatment of patients with hepatitis is supportive and is directed at allowing hepatocellular damage to resolve and repair itself. Effective vaccines are available against hepatitis viruses A and B. Alpha interferons were the first drugs to be approved for the treatment of chronic hepatitis B. (Worman, H.J., 1999). A three-month treatment with interferon therapy induces a response. This is the clearance of the hepatitis B e antigen and serum HBV DNA, normalisation of aminotransferase levels and reduction of necroinflammatory activity in the liver. Several factors have been found to be associated with a favourable response to interferon therapy, the 2 most important being high aminotransferase and low serum HBV DNA levels prior to treatment. These 2 factors reflect endogenous immune clearance of infected hepatocytes (Hussain, M. et al., 1999).

Other treatment options include nucleoside analogues (Worman, H.J., 1999). The main aim of treatment of chronic hepatitis B is to suppress hepatitis B virus replication before there is irreversible liver damage. In the last 5 years, many new antiviral agents have become available such as lamivudine and famciclovir. These have been shown to be safe and effective in inhibiting HBV replication. They inhibit HBV replication by blocking reverse transcription of the (-) strand HBV DNA or synthesis of the (+) strand by HBV DNA. These compounds can be administered orally. Short courses of lamivudine are well tolerated and decrease serum HBV DNA levels in patients with chronic hepatitis B. Famciclovir is well tolerated and can inhibit HBV replication and to improve liver disease in patients with decompensated cirrhosis or recurrent hepatitis B infection after liver transplantation. Several other new antiviral agents have been shown to be effective in inhibiting HBV replication. These include lobucavir, a guanine nucleoside analogue. Lobucavir triphosphate is a potent inhibitor of HBV DNA polymerase acting mainly as a chain terminator. Unfortunately, drug-resistant mutants have been found in some patients who have been on treatment for long durations (Hussain, M. et al., 1999).

There is no vaccine for hepatitis C. Control measures focus on prevention activities that decrease the risks for contracting HCV, including screening and testing blood, plasma and organ donors. Delta hepatitis can be prevented by vaccinating HBV susceptible persons with hepatitis B vaccine (Jawetz et al., 2001). Patients who receive treatment early in the course of chronic hepatitis infections have a better chance of avoiding serious liver damage (Madigan. et al., 2000).

Altogether, the various forms of hepatitis account for over 40,000 illnesses per year. Control of these is based on hygiene and cleanliness measures (Madigan. et al., 2000). The control of the hepatitis virus must continue to be maintained to ensure that the numbers of infected individuals decreases.

References:

Freeman, A.J., Marinos, G., Ffrench, R.A., Lloyd, A.R., 2001. Immunopathogenesis of hepatitis C virus infection. Immunology and cell biology, vol 79, issue 6, Page 515.

Hussain, M., Lok, A.S.F., 1999. Mutations in the hepatitis B virus polymerase gene associated with antiviral treatment for hepatitis B. journal of viral hepatitis, vol6, issue 3, Page 183.

Jawetz, Melnick & Adelberg (2001). Medical Microbiology. 22nd Edition. Appleton & Lange.

Locarnini, S., 2000. Molecular pathogenesis of viral hepatitis. Journal of gastroenterology and hepatology, vol 15, issue s3, Page G46.

Madigan, Martinko & Parker (2000) Brock biology of microorganisms. 9th Edition. Prentice Hall.

Worman, H.J., 1999. Hepatitis B.

Worman, H.J., 1999. Hepatitis C.

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