Hepatitis B is an enveloped double-stranded DNA virus. It is estimated that 1-2% of the New Zealand population are carriers with an especially high carriage rate in Maori and Pacific Islanders. Transmission is via a number of routes, most importantly parenterally, sexually and vertically. The incubation period is long (approximately 6 weeks to 6 months).  The onset of disease is usually insiduous and may be icteric or anicteric.  Symptoms, when present, include anorexia, malaise, nausea, abdominal pain, vomiting, RUQ pain,pale stools, dark urine and jaundice.  Transmission can be via parenteral, sexual and perianal routes.

The Hepatitis B Surface Antigen (HBsAg) is the first serologic marker to appear following HBV infection. Its presence indicates the patient is infectious. Detectable in serum 30-60 days after exposure to HBV, HBsAg generally peaks at or shortly after the onset of elevated liver enzymes (if a symptomatic infection) during the acute phase of the disease. With recovery, HBsAg becomes undetectable and is replaced by the corresponding anti-HBs which confers immunity.

Presence of HBsAg in serum for a period of greater than 6 months defines carriage of the virus. Period of carriage is variable, but it is usually over many years.

Infection in neonates is usually sub-clinical. In children approximately 10% is clinical and adulthood approximately 30-50% clinical. Carriage rates are high when infection is acquired earlier in life (e.g. approximately 90% in childhood and probably <5% in adulthood). Mortality in icteric cases is <1-2%.

DIAGNOSIS:

Serological assays for diagnosis are based on the detection of circulating antigens and antibodies.

1. HBs antigen:  this is a component of the envelope and is the earliest marker of HBV infection. It is present in serum prior to the onset of symptoms. If HBsAg is present in serum for more than 6 months the patient is defined as a "carrier".

2. HBe antigen: this is the next marker detectable. Presence of HBeAg generally indicates high infectivity.

3. HBc antigen: this antigen is only present in liver and therefore not detectable serologically. 

4. Anti-HBs: this antibody develops as HBs antigen declines, therefore there can be a "window" between HBsAg declining to undetectable levels and  anti-HBs rising to detectable levels. Development of anti-HBs implies clearance of the virus and development of immunity. 

5. Anti-HBc: this is the earliest antibody detectable and is usually present with or soon after the onset of clinical symptoms of acute infection (IgM then IgG). Total anti-HBc is measured and anti-HBc IgM. The latter usually becomes negative within 6 months following acute infection. 

6. Anti-HBe: this develops as HBe antigen declines.

n approximately 5% of adults and 70-90% children (< 5 years) a carrier state becomes established, which can lead to significant liver disease.

References

1.      Abbott Laboratories Axsym HBsAg kit product insert.

2.      Hepatitis Learning Guide.

Second Edition. Abbott Laboratories, Abbott Park Illinois USA p 1-63 (1994)

HBV drug resistance

HBV PCR

Quantitative Hepatitis B surface antigen