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Hepatitis B. Epidemiology HBV infection acquired early in life is a major cause of chronic liver disease, including cirrhosis, and primary liver cancer.

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Presentation on theme: "Hepatitis B. Epidemiology HBV infection acquired early in life is a major cause of chronic liver disease, including cirrhosis, and primary liver cancer."— Presentation transcript:

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 2 nd 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 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%

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

13 Phases of Chronic HBV Infection 1.Immune tolerant phase: the immune system doesn’t recognise surface or e antigens and a high viral load (high HBV DNA) persisting for years if infected perinatally or during childhood 2.HBeAg clearance phase: development of anti-Hbe (Hbe-Ag seroconversion) and development of immune response causing: 1.Liver inflammation, raised LFT’s 2.Flare-ups causing jaundice 3.Progression of liver disease to possible advanced liver disease if high viral load HBV DNA > 100,000 IU/mL 3.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 4.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

14 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)

15 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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