Hepatitis D virus (HDV) or delta agent is a virus that only causes hepatitis in conjunction with hepatitis B.
Hepatitis D, a single stranded RNA virus, has a genome which does not encode for its own protein coat. It there-fore has to use proteins made by the HBV. It is therefore not pathogenic in the absence of HBV replication. Unlike HBV, it has a direct cytopathic effect, which may contribute to the clinical features. Any patient at risk of hepatitis B is at risk of hepatitis D, particularly intravenous drug users.
Two patterns of disease are seen:
When hepatitis B and D simultaneously infect the host a co-infection occurs. The resulting hepatitis is of variable severity, but is more likely to cause fulminant hepatic failure. The chronic carrier state is rare.
If hepatitis D occurs in patients carrying hepatitis B, i.e. a super-infection, it may precipitate an acute hepatitis or convert a mild chronic disease to fulminant hepatitis. HDV super-infection has a strong tendency (10–40%) towards chronic progressive disease, leading to an increased risk of rapidly developing cirrhosis and hepatocellular carcinoma.
Finding antibodies to HDV (IgM or IgG) is diagnostic. Alternatively, a cDNA probe can be used to detect HDV in the blood, and HDAg can be detected in liver cells using immunofluoresence.
There is no vaccine for hepatitis D; however, vaccination against hepatitis B will prevent hepatitis D infection. Interferon α can be used to treat patients with chronic hepatitis B who also have hepatitis D infection.
Recovery from hepatitis B leads to clearance of hepatitis D also. However, chronic hepatitis D infection has a poor prognosis.