Time After Exposure

Fig. 22-8 The time course of serological markers in relation to clinical illness in hepatitis D (HDV) infection (A) Coinfection with HDV plus hepatitis B virus (HBV) (B) Superinfection with HDV of an HBsAg canier, leading to chronic HDV infection. ALT, Alanine aminotransferase, anti-HBs, antibody to hepatitis B surface antigen; anti-HDV, antibody to hepatitis D antigen. [From J H. Hoofnagle and A. M. Di Bisceglie, in "Antiviral Agents and Viral Diseases of Man" (G J. Galasso, R J WhiteJy and T C. Merigan, eds ), 3rd Ed , pp 445 and 446. Raven, New York, 1990 ]

line. Total antibody to HDV is demonstrable for longer, but even the IgG response is usually short-lived following resolution of the infection, so screening for antibody is not a reliable indicator of past HDV infection.

In contrast, superinfection by HDV of an HBsAg carrier generally induces a more severe acute disease, after a shorter incubation period, and progresses to chronic active hepatitis and/or cirrhosis. Acute superinfection is distinguished from acute coin feet ion by the absence of anti-HBc IgM. In chronic hepatitis delta infection, alanine aminotransferase levels fluctuate but remain elevated, whereas anti-HD IgM as well as total anti-HD and HDV RNA remain demonstrable in the serum for months or years. Table 22-5 summarizes the patterns of serological markers of HDV infection.

Epidemiology

The world distribution of HDV roughly parallels that of its helper virus HBV, but is more patchy; for example, HDV is rare in the high HBV prevalence countries of east Asia, including most parts of China. High HDV prevalence regions include the western Amazon basin, parts of central Africa, Romania, and isolated provinces in China. In these areas over 20% of HBsAg carriers and over 60% of chronic hepatitis cases have markers of HDV infection. For example, a remote tribe of indigenous Venezuelan Indians has been found to suffer a 10% annual HDV infection rate in HBV carriers, with a high case-fatality rate from fulminant hepatitis or from rapidly progressive chronic hepatitis. Prevalence is moderately high in southern and eastern Europe, the Middle East, the central Asian republics, the Indian subcontinent, and Central and South America. Three genotypes of HDV have been described so far: genotype 1 is widely distributed; genotype 2 is a single isolate from Japan; and genotype 3, from South America, is associated with a severe form of hepatitis D characterised by high mortality and a characteristic histologic lesion in the liver called a morula cell.

Transmission ol HDV occurs by exactly the same routes as does HBV, namely, parenteral, perinatal, sexual, and contact. In developing countries of high HDV prevalence it is likely that most of the spread occurs horizontally among children by contact with open skin lesions, etc., and among adolescents and young adults by sexual intercourse. Perinatal transmission is less common than with HBV. In developed countries of low prevalence, such as North America, temperate South America, Australia, and western and north-

Table 22-5

Serological Markers oí Hepatitis D Infection

Serological marker"

Table 22-5

Serological Markers oí Hepatitis D Infection

Serological marker"

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