Hepatitis D virus (HDV), or delta virus, is a hepatitis B virus satellite that needs empty envelopes of HBV to multiply. It can establish acute and chronic infections in humans. Worldwide, 5 to 20 million individuals are chronic carriers of HDV. HDV infection is associated with significant worsening of HBV-related liver disease.
HDV is transmitted mainly by blood or other body fluids (sperm and vaginal secretions). It shares the transmission modes of HBV: percutaneous and sexual transmission (mother-to-child transmission is rare).
Five to 20 million people are chronic carriers of HDV worldwide, and it is estimated that approximately 5 to 10% of chronic HBV carriers have anti-HDV antibodies. The prevalence of HDV among HBV carriers, however, varies considerably from region to region. France is a region of low prevalence.
There are two modes of delta virus infection: simultaneous infection by HBV and HDV (co-infection) and HDV superinfection in a chronic HBsAg carrier. It is important to distinguish these two situations because their prognosis is very different.
The incubation period varies from three to seven weeks. Acute hepatitis D is usually symptomatic, but the symptomatology is nonspecific. More than 65% of patients develop jaundice (yellow staining of mucous membranes and skin). Simultaneous infection with HBV and HDV (co-infection) can lead to moderate to severe hepatitis, sometimes fulminant, but most often results in a self-limiting disease with elimination of both viruses. The progression to chronic hepatitis D is rare (less than 5% of cases of acute hepatitis). However, superinfection with HDV in a chronic carrier of HBs antigen leads to chronic hepatitis D in more than 90% of cases.
Fulminant hepatitis is 10 times more common in B plus D co-infections than in cases of infection with HBV alone. The risk of death is very high (mortality above 80%) in the absence of liver transplantation.
Chronic hepatitis due to HDV in a chronic HBV carrier is not clinically distinguishable from chronic hepatitis B. Progression to cirrhosis is, however, faster than for isolated chronic hepatitis B and more frequently associated with signs of liver failure. The severity of liver disease is also greater.
Diagnosis is based on the search for total anti-HD antibodies (anti-HD IgG and IgM) in the blood. These antibodies may be present during a chronic infection or may be evidence of an old infection. If they are present, diagnosis requires the search for HDV RNA, the presence of which confirms active infection. The search for markers of HDV infection should be part of the initial assessment in any chronic HBV patient.
Acute delta hepatitis does not require specific treatment. Interferon alpha is still the only recommended treatment strategy for patients with chronic delta hepatitis. Its results are mostly modest and transient.
Vaccination against hepatitis B is the main, indirect, means of hepatitis D prevention, since subjects protected against HBV cannot be infected with HDV.
