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.
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
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.
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.
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.
are 36-43 nm in size. They are roughly spherical and enveloped,
with no distinct nucleocapsid structure, though they may be icosahedral.
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.
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.
replication is not acutely cytopathic, and both humoral and cellular
immune mechanisms may be involved in the pathology of hepatitis
transmitted percutaneously or sexually through contact with infected
blood or blood products.
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.
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.
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.
of HDV infection can be achieved by targeting and limiting HBV infections.
HBV vaccination is therefore recommended to avoid HBV-HDV coinfection.
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.