The prognosis is excellent, with most patients making a complete recovery. The mortality in young adults is 0.1% but it increases with age. Death is due to fulminant hepatic necrosis. During convalescence 5-15% of patients may have relapse of the hepatitis but this settles spontaneously. Occasionally a more severe jaundice with cholestasis will run a prolonged course of 7-20 weeks and is called cholestatic viral hepatitis.
There is no reason to stop alcohol consumption other than for the few weeks when the patient is ill. Patients may complain of debility for several months following resolution of the symptoms and biochemical parameters.
This is known as the posthepatitis syndrome; it is a functional illness. Treatment is by reassurance. HAV never progresses to chronic liver disease.
There is no specific treatment; rest and dietary measures are unhelpful. Corticosteroids have no benefit. Admission to hospital is not usually necessary. The condition is notifiable in the UK.
PREVENTION AND PROPHYLAXIS
Control of hepatitis depends on good hygiene. The virus is resistant to chlorination but is killed by boiling water for 10 min. Ideally all individuals should have anti-HAY antibody tests to assess their requirement for prophylaxis.
ACTIVE IMMUNIZATION using a formaldehyde inactivated vaccine is commercially available. This is now preferable
to repeated immunoglobulin injections for people frequently travelling to endemic areas.
PASSIVE IMMUNIZATION. Normal immunoglobulin (0.04-0.06 rnl kg-l i.m.) gives protection for 2-3 months and is useful for persons at risk.
The virus (HBV) is present worldwide and has infected more than 2000 million people. There are an estimated 350 million carriers. The UK and the USA have a low prevalence but it rises to 10-15% in parts of Africa, the Middle and the Far East.
Spread of this virus is by the intravenous route, e.g. transfusion of infective blood or blood products, by contaminated needles used by drug addicts, tattooists or acupuncturists, or by close personal contact, e.g. sexu.al intercourse, particularly in male homosexuals. The VIrUScan be found in semen and saliva. Vertical transmission from mother to child during parturition or soon after birth is the most important means of transmission worldwide. The role of insect vectors is controversial; there is no evidence that HBV replicates in these insects but the virus has been detected in mosquitoes and bed bugs.
Hepatitis B virus
Under electron microscopy a number of particles are seen. The whole virus is the Dane particle, which consists of an inner core formed by the liver cell nucleus and an outer surface coat (HBsAg) produced by multiplication in the cytoplasm. The inner core contains doublestranded DNA, DNA polymerase, the core antigen (HBcAg) and the e antigen (HBeAg). Small spheres and tubules (100 nm long) of excess surface antigen protein are also produced.
The virus only replicates in the liver. The core antigen enters and replicates in the nucleus and eventually becomes integrated with the host nuclear DNA. The host DNA polymerase then transcribes for the virus. This may be an important link in the development of hepatocellular carcinoma. HBsAg particles have further antigenic determinants on their surface known as a, d, y, w and r. Combinations of these subdeterminants, e.g. adw, adr, ayw and ayr, are useful in epidemiology for studying geographical patterns of infection.
Hepatitis B mutants
Mutations are being increasingly described in the vanous reading frames of the HBV genome. These mutants can emerge in chronic HBV carriers or can be acquired by infection. These variants of the HBV genome have also been found in patients with fulminant and fatal hepatitis who have HBsAg and anti-HBe rather than. the e antigen itself. The amino acid sequence of the e antigen protein is almost identical to that of the core antigen which is involved in viral replication. Separate messenger RNAs have not been described for the two antigens but HBeAg is initiated several nucleotides upstream of HBcAg. A guanosine (G) to adenosine (A) mutation in the precore region of the genome creates a stop codon (TAG) that prevents the production of HBeAg but the synthesis of HBcAg is unaffected. Mutants have also been seen following interferon therapy. Their existence means that serological markers such as the HBeAg are less useful in detecting infectivity and HBV DNA must be measured.