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Chapter: Microbiology and Immunology: Virology, Virus: Arboviruses

Hepatitis D Virus

Hepatitis D virus is the smallest of known human pathogens that causes infections in humans.

Hepatitis D Virus

Hepatitis D virus is the smallest of known human pathogens that causes infections in humans. It is an RNA virus, which is structur-ally unrelated to hepatitis A, B, or C virus. Hepatitis D virus is unique in being an incomplete virus and requires the presence of HBV to replicate and infect other hepatocytes. Hence, HDV infec-tion occurs only in those patients who suffer from HBV infection.

        Hepatitis D virus was first reported by Rizzetho and col-leagues in Italy in 1977. They demonstrated the viral antigen in nuclei of hepatocytes of patients infected with HBV and suggested it to be a new hepatotropic virus delta, or HDV.

Hepatitis D virus is a spherical, enveloped virus measuring 85 nm in diameter. It contains a single-stranded negative-sense 1.7 kb RNA. In blood, HDV or delta agent contains delta Ag (HDAg) surrounded by HBsAg envelope. HBsAg is required for HDV replication, but it may be suppressed to undetect-able levels with active HDV replication. The single-stranded RNA is circular and is surrounded by delta-antigen core, which in turn is surrounded by an envelope which contains HBsAg. Delta antigen may occur in two sizes—small (24 kDa) or large (26 kDa). Delta antigen is the only protein coded for HDV RNA, and it is distinct from antigenic determinants of HBV.

    Hepatitis D virus causes a more rapid and severe disease with rapid progression in HBV carriers superinfected with delta and HBV. Delta agent replicates in the liver, causing liver damage and cytotoxicity. Chronic HBV carriers superinfected with HDV usually also develop chronic HDV infection. Chronic coinfection often leads to a rapidly progressive subacute or chronic hepatitis, resulting in more rapid progression to cir-rhosis. Delta agent causes damage to liver cells as a result of direct cytopathic effect in combination with underlying immu-nopathology of HBV disease.

Hepatitis D virus causes an acute and chronic inflammatory disease of liver. Although HDV can replicate independently within the hepatocytes, it requires HBsAg for its propagation. Death of hepatocytes in the liver may occur as a result of direct cytotoxic effect of HDV or through a host-mediated immune response.

Hepatitis D virus is distributed worldwide. It is believed to infect approximately 15 million (5%) of world’s 300 million HBsAg carriers. The highest prevalence of HDV has been reported in Italy, North Africa, Middle East, West Africa, and central Asia including China, Japan, Taiwan, and Myanmar. The infection is most common among adults and children. It is observed more commonly among patients with history of intravenous drug users.

Hepatitis D virus, like hepatitis B virus, is a blood pathogen and is transmitted mostly by blood and vaginal secretions. It is most commonly transmitted by nonpercutaneous routes, especially by close intimate contact in endemic areas of Mediterranean countries. Infection appears to be more commonly transmitted through contaminated blood and blood products in nonendemic areas of northern Europe and North America. Sharing of contaminated needles in intravenous drug users is believed to be the most common method of transmitting HDV. The sexual and perinatal transmission of HDV is also described. Intravenous drug use and multiple blood transfu-sions are the important risk factors for parenteral transmission of the disease.

The incubation period varies from 21 to 45 days but may be shorter in cases of superinfection. The clinical course of disease caused by HDV is varied and ranges from acute self-limited infection to acute fulminant liver failure. Clinically, HDV infec-tion is indistinguishable from other forms of viral hepatitis. Patients coinfected with HBV and HDV show a more severe course of the disease than those infected with HBV alone. Complete clinical recovery and clearance of HBV and HDV coinfection is the most common outcome.

Nearly 1% of the patients with coinfections progress to develop fulminant hepatitis resulting in more rapid progres-sion to cirrhosis. Laboratory diagnosis of HDV infection is usually carried out by serological as well as molecular tests:    

·            ELISA for HDV antigen is usually positive in 20% of patients.

·           IgM ELISA for demonstration of anti-HDV IgM is positive in early stage of infection, whereas IgG ELISA for anti-HDV

·           IgG is positive during later course of infection.

·           Serum antibodies against HDAg are almost exclusively associated with chronic HDV infection.

·           Reverse transcriptase-PCR (RT-PCR) is the most sensitive method (90%) for detection of HDV RNA in blood in the stage of coinfection.

·           In superinfections, high level of both IgM and IgG anti-bodies as well as high level of HDAg and HDV RNA is demonstrated.

No specific therapy is available for treatment of HDV infection of liver. Lamivudine and ribavirin appear to be ineffective against HBV and HDV coinfection. Antiviral therapy with interferon is also ineffective in patients with chronic infections.

Vaccination with HBV vaccine protects against subsequent HDV infection. HDV virus is prevented best in the patients already infected with HBV by avoiding the use of HDV-contaminated blood or blood products.

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