HDV is found in nature only as a coinfection with HBV. It is significant because its presence results in more severe acute disease, with a greater risk of fulminant hepatitis and, in chronically infected patients, a greater risk of cirrhosis and liver cancer.

A. Structure and replication

 HDV does not fall into any known group of animal viruses. It has a circular, single-stranded RNA genome with negative polarity that codes for one protein (delta antigen), with which the genome is complexed in the virion (Figure.1). In the infectious particle, the nucleoprotein complex is enclosed within an envelope containing HBV-coded HBsAg. Thus, HDV requires HBV to serve as a helper virus for infectious HDV production. The HDV RNA genome is replicated and transcribed in the nucleus by cellular enzymes, whose specificity is probably modified by complexing with the delta protein. [Note: This phase of HDV replication is independent of HBV, whose only helper function is to supply HBsAg for the envelope.]

Fig1. Structure of hepatitis D virus. HBsAg = hepatitis B surface antigen.

B. Transmission and pathogenesis

 Because HDV exists only in association with HBV, it can be transmit ted by the same routes. However, it does not appear to be transmitted sexually as frequently as HBV or HIV (human immunodeficiency virus). Pathologically, liver damage is essentially the same as in other viral hepatitides, but the presence of HDV usually results in more extensive and severe damage.

C. Clinical significance

 HDV disease can occur in one of three variations (Figure 2). First, simultaneous primary coinfection with both HBV and HDV can cause an acute disease that is similar to that caused by HBV alone, except that, depending on the relative concentrations of the two agents, two successive episodes of acute hepatitis may occur. The risk of fatal fulminant hepatitis caused by the presence of HDV is also considerably higher than with HBV alone. The likelihood of progression to the second variation of HDV disease (chronic coinfection with HBV) is greatly increased as well. In this case, cirrhosis and HCC or death due to liver failure also develop more frequently than with HBV infection alone. The third variation, primary HDV infection of a chronically HBV infected individual, leads to an episode of severe acute hepatitis after a short incubation period and develops into chronic HDV infection in more than 70 percent of cases. Again in this situation, the risk of acute hepatitis becoming fulminant is greatly increased, and the persistent infection is often the severe chronic type.

Fig2. Consequences of hepatitis D virus (HDV) infection. HBV = hepatitis B virus.

D. Laboratory identification

 The immunologically based methods used to diagnosis HBV are also applied to HDV. The delta (D) antigen and immunoglobulin M antibodies against it can be detected in serum. The presence of HDV RNA in serum or liver tissue, as detected by hybridization with or without the use of reverse transcriptase and polymerase chain reaction amplification, is an indicator of active infection.

E. Treatment and prevention No treatment specific for HDV infection is available. Because HDV depends on coinfection with HBV, the approaches for preventing HBV infection are also effective in preventing HDV infection. There is no vaccine specifically for HDV. Therefore, those who are chronically infected with HBV can only be protected from HDV infection by limiting chances for exposure. Those who are protected against HBV infection through vaccination will not be affected by HDV.

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غوغل في مأزق.. بيانات 2.5 مليار مستخدم بقبضة القراصنة

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مواضيع ذات صلة

Hepadnaviridae

Poxviridae

West Nile Virus

Epstein-Barr Virus

Herpes simplex virus, types 1 and 2

Herpesviridae: Structure and Replication

Adenoviridae

Human Cowpox

Human Monkeypox

Smallpox virus

Papovaviridae: Subfamily Polyomavirinae

Effects of viral infection on the host cell