Delta Hepatitis

The hepatitis delta virus (HDV) is a defective RNA virus which is capable of replication only during concomitant infection with HBV. Thus it occurs only in patients who have HBsAg in the serum. It was discovered by immunofluorescent staining as a nuclear antigen distinct from the antigens of HBV, and is found in hepatocytes and serum of infected individuals. The hepatitis delta virus is a 35 nm particle which has an external coat of HBsAg provided by the genome of HBV (the helper virus) and an internal delta antigen (HDV-Ag) provided by the genome of HDV. The genome of HDV is smaller than that of any animal virus, and resembles that of the viroids of plants.

The virus can cause either acute or chronic hepatitis. Acute delta hepatitis resembles other forms of acute hepatitis, but is more severe, with a case fatality rate of 2-20% (compared with less than 1% in acute hepatitis B). Chronic delta hepatitis is also more severe than other forms of chronic viral hepatitis; 70-80% of patients develop cirrhosis with portal hypertension. Acute delta hepatitis occurs as either coinfection or superinfection. Coinfection is the simultaneous occurrence of acute hepatitis B and acute delta infection. Superinfection is the occurrence of acute HDV infection in a chronic HBV carrier. Acute delta coinfection is usually mild and self limited, rarely leading to chronic hepatitis. In contrast, acute delta superinfection leads to chronic hepatitis in more than 80% of patients.

Diagnosis of delta hepatitis is made by detecting antibodies to HDV in the serum of a patient who has HBsAg-positive hepatitis. Delta hepatitis should be suspected in any patient with acute or chronic hepatitis B infection, especially if the disease is severe or fulminant, or if the patient has a history of intravenous drug abuse or repeated exposure to blood or blood products. Clinical features suggesting delta infection are a biphasic illness in acute hepatitis or a history of jaundice or worsening of disease during the course of chronic hepatitis B infection.

Delta hepatitis occurs in three epidemiological settings. Endemic infection is especially common in the Mediterranean area and in the Middle East. The highest prevalence is reported from Kuwait and Saudi Arabia, where 20-40% of HBsAg carriers have antibody to HDV. Delta hepatitis is rare in northern Europe, the United States and most of South America, and is also uncommon in southeast Asia and China, where the prevalence of chronic HBV infection is very high. The disease occurs in epidemic form in isolated populations in certain underdeveloped areas of the world, especially in northern South America and the Amazon Basin. In these outbreaks the disease is strikingly severe, with sudden onset of fulminant hepatitis and a rapidly fatal course. The epidemic form occurs most frequently in children. In northern Europe and the United States delta hepatitis occurs primarily in certain high risk groups, including intravenous drug addicts and patients who receive multiple blood transfusions or antihaemophilic globulin. Although sexual transmission of delta hepatitis can occur, it is rare in most but not all populations of male homosexuals.

Immunization against HBV infection also provides immunity against delta hepatitis. Unfortunately there is no way to prevent HDV superinfection in HBsAg carriers, other than avoidance of contact. There is no established therapy for delta hepatitis. Corticosteroids are not effective in modifying the course or preventing progression of the disease. Alpha interferon inhibits replication of HDV and has produced clinical improvement in some patients, although discontinuation of therapy appears to be followed by relapse in nearly all cases. Results of liver transplantation in chronic delta hepatitis have been good, and some long-term survivors have remained both HBsAg- and HDV-negative after transplantation.