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Hepatitis Delta Agent

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Hepatitis Delta Agent is not a member of hepadnaviridae. However, it works along with hepatitis B to cause infection. A satellite of hepatitis B virus, hepatitis delta agent is a defective RNA virus which requires the help of a hepadnavirus like HBV for its own replication.


The hepatitis delta virus is present worldwide and in all age groups. Its distribution somewhat parallels that of HBV infection, however, its prevalence rates vary by country. Russia, Romania, Southern Italy and the Mediterranean countries, Africa, and South America have the highest HDV prevalence rates, whereas countries such as China have disproportionately low rates of HDV infection.

Structure & Genome

The genome of HDV is unrelated to the genomes of hepadnaviruses. HDV is not a defective interfering particle, but rather a satellite virus, a natural subviral satellite of HBV.

HDV is replication defective. It requires the surface antigen of HBV for the encapsidation of its own genome. The envelope proteins on the outer surface of HDV are entirely provided by HBV.

The internal nucleocapsid structure of HDV is composed of the viral single-stranded RNA genome and about 60 copies of delta antigen, the only HDV-encoded protein, in its large and small form.

HDV virions are 36-43 nm in size. They are roughly spherical and enveloped, with no distinct nucleocapsid structure, though they may be icosahedral.

The HDV genome is a single, negative-stranded, circular RNA molecule that is about 1.7 kb in length. HDV can be classified into three genotypes, which are associated with different geographic locations and vary in severity of disease.


HDV does not infect established tissue culture cell lines. Complete viral replication cycles in vitro are limited to primary hepatocytes (of woodchucks or chimpanzees), that are coinfected with hepadnavirus or cotransfected with hepadnavirus cDNA. In nature, HDV has only bene found in humans infected with HBV.

HDV genome replication is not acutely cytopathic, and both humoral and cellular immune mechanisms may be involved in the pathology of hepatitis D.


HDV is transmitted percutaneously or sexually through contact with infected blood or blood products.

Risk Groups

Chronic HBV carriers are at risk for infection with HDV. Individuals who are not infected with HBV but are susceptible to infection with HBV are also at risk of simultaneous or subsequent infection with HDV. HDV inoculation in the absence of HBV will not cause hepatitis D, since HDV requires the support of the hepadnavirus for its own replication. Alone, the HDV viral genome replicates in a helper-independent manner, but virus particles are not released.

Clinical Consequences

Infection with both HBV and HDV is associated with more severe liver injury than HBV infection alone. HDV infection of chronically infected HBV carries may lead to fulminant acute hepatitis or chronic active hepatitis, often progressing to cirrhosis. Chronic HDV infection may also lead to the development of hepatocellular carcinoma.


There is currently no effective antiviral therapy available for treatment of acute or chronic type D hepatitis. Antivirals such as acyclovir, ribavirin, lamivudine, and synthetic analogues of thymosin have proved ineffective. Immunosuppressive agents are not effective in treating Hepatitis D either. High doses of interferon have yielded remissions in infected patients. However, these patients remain positive for HDV RNA despite their improved clinical conditions. Liver transplantation is often recommended for treating fulminant acute and end-stage chronic hepatitis.


Control of HDV infection can be achieved by targeting and limiting HBV infections. HBV vaccination is therefore recommended to avoid HBV-HDV coinfection.

There is no effective measure to prevent HDV infection of chronic HBV carriers, and prevention of HBV-HDV superinfection can only be achieved through education to reduce risk behaviors.



The World Health Organization. “Hepatitis D.” 2002.