Globally, viral hepatitis is probably the commonest of all serious viral infections. In the Eastern Mediterranean Region hepatitis infections constitute a major public health problem in terms of morbidity, mortality and severe liver diseases, including cirrhosis and hepatocellular carcinoma.
According to the conventional classification, this group of infections includes viral hepatitis A, viral hepatitis B, delta hepatitis. and non-A, non-B viral hepatitis.
The subgroup non-A, non-B viral hepatitis was, until recently, diagnosed by exclusion. It was known to consist of two forms - parenterally transmitted and enterically transmitted. The parenterally transmitted form is now known to be mostly due to infection with hepatitis C virus (HCV), which was cloned for the first time in 1989 (another transmissible agent may account for cases of acute non-A, non-B, non-C hepatitis with parenteral risk factors). The enterically transmitted form is now known to be due to infection with hepatitis E virus, which was cloned and described for the first time in 1990, although it had long been suspected to be the cause of large waterborne epidemics.
Viral hepatitis C. Many of the clinical and epidemiological features of viral hepatitis C infection have been clarified over the past few years, especially since the isolation and cloning of the causative virus and the development of laboratory tests for its detection.
Clinical features. Most cases of acute HCV infection are asymptomatic with normal liver function tests. Symptomatic cases progress to jaundice less frequently than hepatitis B, and when they do so are clinically indistinguishable from other causes of viral hepatitis. A positive diagnosis of acute viral hepatitis C can be made by detecting seroconversion to anti-HCV positivity. Many infected people remain carriers of the virus, with various degrees of hepatocyte damage and fibrosis. Chronic hepatitis follows acute viral hepatitis C infection in 64-88% of cases. The role of long-term infection with HCV in chronic hepatitis has been demonstrated in various studies, which found evidence of HCV infection in 60-100% of patients with chronic hepatitis when other causes were excluded. The highest rates occur in Japan and Mediterranean countries. Most cases of HCV chronic hepatitis probably follow an indolent course; however, at least 20% of such cases ultimately develop liver cirrhosis and among these many progress to hepatocellular carcinoma.
HCV infection can be detected either by demonstrating anti-HCV positivity or HCV RNA in blood samples. The sensitivity of first-generation enzyme-linked immunosorbent assays (ELISA-1) for detecting antibodies to HCV was relatively low, especially for the general population not at high risk and for the early recognition of acute disease (seroconversion occurs 2-26 weeks after the onset of hepatitis). Such assays also lacked specificity.
The second-generation assays (ELISA-2) have increased sensitivity for diagnosing both acute and chronic hepatitis C infection, and in addition have improved specificity. The third-generation assays have so far not exhibited any improvement over the second-generation. The results of screening assays are usually confirmed using recombinant immunoblot assays (RIBA), two generations of which are available. HCV RNA is detected using the polymerase chain reaction (PCR); demonstration of the presence of detectable virus sequence is, however, a better predictor of infectivity.
The above-mentioned screening tests are both more sensitive and more specific than indirect markers of infection. including alanine aminotransferase levels and antibody to hepatitis B core antigen, which are already used for this purpose. However, the high cost of these newer screening tests precludes their use in many developing countries.
Liver transplantation is the only currently available therapy for HCV patients with advanced progressive liver disease, cirrhosis and potentially life-threatening complications. …