Abstract

HDV is the causative agent of hepatitis D and is associated with both acute and chronic hepatitis. HDV infection occurs worldwide, and the prevalence is reported to be highest in the Mediterranean region, the Middle East, central and northern Asia, west and central Africa, Taiwan, and the Amazon basin. HDV requires the helper function of HBV to provide the hepatitis B surface antigen to complete its life cycle. The complete infectious virion is composed of an outer lipoprotein envelope, consisting of small, middle, and large hepatitis B surface antigen, that surrounds an inner ribonucleoprotein. The ribonucleoprotein consists of the small and large hepatitis delta antigen complexed to the viral genome. Eight major genotypes have been reported. Clinically, acute HDV infection may occur either as a coinfection simultaneously with HBV or as a superinfection in which HDV infection is superimposed in a person with chronic HBV infection. Most cases of acute HDV coinfection resolve spontaneously, whereas most cases of acute HDV superinfection become chronic. The natural history of chronic HDV infection is variable, ranging from mild chronic hepatitis to severe hepatitis with rapid progression to cirrhosis and hepatic decompensation. Chronic HDV infection is associated with an increased frequency of cirrhosis, HCC, and mortality compared with chronic HBV infection. There is no effective treatment for chronic HDV infection; peginterferon α may be used in selected cases. Several promising host targeting agents with demonstrable antiviral activity are in development. LT remains an option for patients with decompensated cirrhosis.

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