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Hepatitis B

Hepatitis B. Epidemiology. HBV infection acquired early in life is a major cause of chronic liver disease, including cirrhosis, and primary liver cancer The hepatitis B virus is the 2 nd most important known human carcinogen, after tobacco

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Hepatitis B

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  1. Hepatitis B

  2. Epidemiology • HBV infection acquired early in life is a major cause of chronic liver disease, including cirrhosis, and primary liver cancer • The hepatitis B virus is the 2nd most important known human carcinogen, after tobacco • Up to 400 million people, mostly in the Asia Pacific region, are chronically HBV– infected

  3. Australia • There is currently an epidemic of chronic Hepatitis B in Australia • In Australia up to 160,000 are chronically infected with HBV – half are from endemic countries of the Asia Pacific region • Unlike HIV and Hep C (sexy infections) there is no comprehensive national Hepatitis B public health strategy • Universal hepatitis B vaccination for infants and people at high risk of infection has been implemented in Australia since 2000

  4. Australia

  5. At Risk Groups in Australia • IV drug users (16% of prevalence but 40% of all new acute cases. Usually co-infected with hepatitis C increasing risk of chronic illness and advanced liver disease) • People born in an endemic region • Asia and the Pacific Islands (50% of prevalence) • Africa, the Middle East, and the Mediterranean region • Homosexual men (8%) • Indigenous - the virus was discovered in 1965 in Australian aborigines. They make up 2% of the total population but 16% of the total prevalence of chronic hepatitis B. • Prisoners

  6. At Risk Groups in Australia

  7. Transmission of HBV • Saliva, semen, blood • Perinatal – risk of disease is 80% from mother +ve to HBsAg and HNeAg • To children through household contact • In healthcare settings and sharing of contaminated equipment

  8. Age Determimes Course of Illness

  9. Virology • Hep B is a DNA virus and uses reverse transcription to copy its DNA • The virus does not kill cells but expression of antigens causes both cytotoxic CD8+ T cell lysis (minor defence) and secretion of cytokines (IFN-γ and TNF-α ) causing non-cytolytic viral inhibition (major defence) see http://www.jimmunol.org/content/184/1/287 • The antigens expressed by infected hepatocytes are: • Surface antigen • Core antigen • E antigen (a soluble protein secreted by the virus into the bloodstream)

  10. Acute HBV Infection - Clinical • Symptoms: primarily jaundice after 8 weeks (range 6-12 weeks) but other symptoms can appear such as malaise, nausea, vomiting, LOA, arthralgia, myalgia • Serological markers • HBV DNA early marker (2 weeks after infection) • HBs-Ag can be detected 1 month after infection • anti-HBc IgM and Hbe-Ag at 8 weeks • LFT’s: ALT, AST • Mortality is 1%

  11. Chronic HBV Infection - Clinical • Defined clinically by serological markers: HBs-Ag persisting for longer than 6 months • Other markers are usually variable

  12. Phases of Chronic HBV Infection • Immune tolerant phase: the immune system doesn’t recognise surface or e antigens and a high viral load (high HBV DNA) persisting for 20-30 years if infected perinatally or during childhood • HBeAg clearance phase: development of anti-Hbe (Hbe-Ag seroconversion) and development of immune response causing: • Liver inflammation, raised LFT’s • Flare-ups causing jaundice • Progression of liver disease to possible advanced liver disease if high viral load HBV DNA > 100,000 IU/mL • Low/non replicative phase: almost complete eradication of the virus with normal LFT’s and low HBV DNA, minimal liver damage and low risk of developing advanced live disease • Reactivating phase: immunosuppression typically is the cause of reactivation of the infection, inflammation and raised ALT/AST with increasing HBV DNA but no return of Hbe-Ag. Advance liver disease can develop if HBV DNA is > 100,000 IU/mL

  13. Treatment of Hep B • The targets of treatment are: • Inhibit viral DNA replication • Enhance the immune response (as already mentioned, the main immune response is the non-cytolytic one involving cytokines)

  14. Ongoing Treatment • Medicare only pays for monotherapy, which is suboptimal - cf successful combination therapies subsidised for “sexier” Hep C and HIV • Nucleoside monotherapy has been associated with development of resistance • LFT’s and serology are performed every 3 months to determine effectiveness of treatment (not covered by Medicare)

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