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Indian Journal for the Practising Doctor

Vol. 5, No. 6 (2009-01 - 2009-02)


With a world obsessed with HIV/AIDS, parenteral hepatitis (B, C, D & G) is not getting the attention it merits. We know that hepatitis B is almost 100 times more common and as many times as infectious as HIV, still complacency remains. For the sake of comparison even hepatitis C affects four times more people than HIV does. More than 2 billion people (ie 1/3 of the entire population of the world) have already suffered from hepatitis B, of which 350 million have turned in to highly infectious chronic carriers. An estimated 150-200 million are infected with hepatitis C, the vast majority of them becoming chronic carriers, since only a maximum of 30% can be cured. Hepatitis B can be prevented by routine screening of blood before transfusion and by a very effective, economical vaccine available everywhere now. We are aware that, in India, hardly 30% of the transfused blood is screened for HIV, HBV, Syphilis & Malaria. Hepatitis C, transmitted primarily by blood, is of particular concern since no screening is available for the donated blood.

Although liver injury is chemically evident in all patients, the majority are asymptomatic and anicteric; only 25–40% of the patients develop malaise, weakness and anorexia, and some become icteric. Therefore, the infection is hardly diagnosed till chronic stage has set in. There is no vaccine to prevent it and treatment success rate ranges between 10 and 30%.

Unlike hepatitis B, which is self-limiting in the majority, hepatitis C is self-limited in only 15% of the patients. Almost 85% of patients fail to clear the infection by six months and develop chronic hepatitis with persistent (or sometimes intermittent) viremia. This implies that in most of the cases, HCV leads to severe liver disease, and even in countries where liver disease resulting from hepatitis B is largely prevented, hepatitis C is becoming the leading cause of severe liver disease requiring liver transplant. A myriad of extra-hepatic complications may also occur with hepatitis C. Thus, unlike its bigger brother HBV which is essentially hepatotrophic, hepatitis C has a bigger agenda of disrupting other systems including the immunity.

Unlike the hepatitis B virus, HCV is genetically heterogeneous; till date 6 genotypes and over 120 subtypes have been identified, and more are in the process of being characterized. Numerous subtypes of genotype 3 are found in India, a pattern reflective of long-standing endemic infection. Contrary to this, although one or more types are present in other parts of the world, each is represented by few subtypes, suggestive of recent transmissions. This implies that though we were late to recognize the true devastating potential of hepatitis C in this country, the virus was silently busy consolidating its position.

Despite significant progress in the field of biotechnology, reliable diagnostic procedures, an alternative animal model other than the chimpanzee, an efficient cell culture that can support long-term replication of the virus and effective therapeutic strategies are still lacking. Therefore, hepatitis C is getting more prevalent by the day, and experts fear that the next pandemic may be caused by hepatitis C!

We console ourselves that HCV is spread by blood transfusion (and through injectable drug abuse, contaminated syringes, needle stick accidents) and in nosocomial settings. Transmission by sexual route, though widely recognized for HBV, has been debatable in case of HCV. Many recent American studies, however, have suggested a 10-20% transmission through sexual activities. Dentists practising oral surgery, practitioners of folk medicine and those involved in hairdressing, ear- or nose-piercing and tattooing are also at higher risk for HCV. High prevalence rates are found in Southeast Asian countries, including India, which sharply contrasts with low prevalence rates in the UK & USA. Studies in New Delhi & Hyderabad showed HCV infection in voluntary blood donors ranging between 1.85% and 2.5%.

Hepatitis C was recognized 3 decades back (1979) and the identification and molecular characterization of HCV was done in 1989. Since then a variety of diagnostic tests based on the detection of either the anti-HCV antibodies or HCV-RNA in patient sera have been developed. Presently, a third-generation ELISA is available in the market; its major drawback is that it fails to differentiate between active and post-infection cases. Also, it cannot be used to detect the infection in Indian patients owing to genotype variations. To overcome this problem, sensitive and cost effective diagnostic peptide-based enzyme immunoassays (EIA) designed to detect HCV infection in Indian patients have been developed.

In addition to novel types, almost all the reported genotypes of HCV are present in India. Thus monitoring of HCV genotypes in India on a regular basis becomes imperative. Trends of the infection in most states is not known. In summary, HCV is a formidable challenge for our country – far bigger than HIV or even HBV. Yet we are not awakening to the danger. In a study conducted by our research personnel we found HCV in sweepers of a rural hospital. That speaks a lot about the ‘universal precautions’ we take.

February 2009
Bashir Gaash

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