Different types of viral hepatitis

Hepatitis A Virus:

HAV is a picornavirus. It has a single serotype, as only one epitope is immunodominant. It is excreted in the faeces of infected persons for about 2 weeks before the onset of the illness and for up to 7 days after.

The disease is maximally infectious just before the onset of jaundice. HAV particles can be demonstrated in the faeces by electron microscopy.

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 produced by multiplication in the cytoplasm.

The inner core contains double stranded DNA, DNA polymerase, the core antigen and the e antigen. Small spheres and tubules of excess surface antigen protein are also produced. The virus 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 sub determinants, eg adw, adr and ayw and ayr are useful in epidemiology for studying geographical patterns of infection.

Hepatitis D:

This is caused by the hepatitis D virus. It is an incomplete RNA particle enclosed in a shell of HBsAg. It is unable to replicate on its own but is activated by the presence of HBV.

It is particularly seen in intravenous drug abusers but can affect all risk groups for HBV infection. Active HBV synthesis is reduced by delta infection and patients are usually HBeAg and HBV DNA negative.

Hepatitis E:

Hepatitis E virus is an RNA virus which causes enteral hepatitis. Epidemics have been seen in many developing countries. It has mortality from fulminant hepatic failure of 1-2 percent which rises to 20 percent in pregnant women there is no carrier state and it does not progress to chronic liver disease.

Serological tests for HEV are being developed although HEV RNA can be detected in the serum or stools by PCR. Prevention and control depend on good sanitation and hygiene.

Hepatitis C Virus:

HCV is a single stranded RNA virus arranged into structural and non structural regions. There are six subtypes based on differences in the non structural region.

Only types I,II and III are seen in Europe and type IV occurs in the Far Est. Immunogenic peptides have been derived from these regions for use in HCV assays and are becoming increasingly sensitive. The concentration of viral antigens in the blood is very low.

Although some histological features are suggestive of the aetiological factor, most of the changes are essentially similar whatever the cause. Hepatocytes show degenerative changes undergo necrosis and are rapidly removed.

The distribution of these changes varies somewhat with the aetiological agent, but necrosis is usually maximal in zone 3. The extent of the damage is very variable between individuals affected by the same agent, at one end of the spectrum.

Single and small groups of hepatocytes die while at the other end multiple acini are destroyed resulting in fulminant hepatic failure. Between these extremes there is limited confluent necrosis of hepatocytes with collapse of the reticulin framework resulting in linking between the central veins the central veins and portal tracts and between the portal tracts.

Centracinar cholestasis is common, but fatty change is usually absent apart from certain types of hepatitis due to toxins such as alcohol or that seen in pregnancy. The extent of the inflammatory infiltrate is also variable, but portal tracts and lobules are infiltrated mainly by lymphocytes.

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