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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 The hepatitis B virus is the 2 nd most important known human carcinogen, after tobacco

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  • 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


  • 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

At risk groups in australia
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

Transmission of hbv
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

Age determimes course of illness
Age Determimes Course of Illness


  • 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)

Acute hbv infection clinical
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%

Chronic hbv infection clinical
Chronic HBV Infection - Clinical

  • Defined clinically by serological markers: HBs-Ag persisting for longer than 6 months

  • Other markers are usually variable

Phases of chronic hbv infection
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

Treatment of hep b
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)

Ongoing treatment
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)