Once a more or less reliable test for HCV was developed, the extent of the problem could be examined, and the results were startling: hepatitis C was everywhere, no matter what population was screened. Estimates of worldwide infection are as high as 240 million.

Developing countries have the highest rates, but rates in North America and western Europe are higher than in eastern Europe. Epidemiologists have theorized that the higher rates in the United States might be accounted for by the large number of immigrants from areas of high prevalence, and by the widespread use of illegal injection drugs. American military involvement in Asia during world war II, the Korean war, and the vietnam war may also be a factor. There is some evidence that cases of liver disease are increasing among patients admitted to veterans administration hospitals. The internationalization of the blood supply undoubtedly helped spread the illness as well. The CDC estimates that 300,000 U.S. citizens were exposed via infected blood products before 1992, when screening of blood for HCV antibodies began.

A trojan horse

HCV, like HIV has to be inside the cell before it can replicate. (However, unlike HIV, HCV is not a retrovirus.That is, it does not incorporate its genetic structure into the cell it invades.) In a sense, HCV fools the body’s immune system into allowing it to pass through the cell wall, and then once inside starts reproducing and causing disease. And it has another nasty trick: it varies its appearance so that the immune system is constantly faced with new challenges. The virus, in other words, is not a single entity, but a family of viruses with different genetic structures and different subtypes. Various strains of the virus can exist not only in different infected people but even within the same person. This gives the immune system a serious challenge: it must respond not to one virus, but to different forms of the same virus. This multipronged attack usually results in victory for the virus, and defeat for the immune system. Scientists now believe that this trick of varying its appearance is what gives the HCV virus the ability to cause such persistent chronic infection, essentially changing its form every time the immune system devises a response to it. Moreover, it may be that, as with HIV even more new and resistant strains begin to develop when drugs are used to attack HCV.

There are now six large groups of HCV, called types or genotypes, labeled 1 through 6. Each of these genotypes contains many subtypes (more than ninety have been discovered), called 1a, 1b, 2a, 2b, and so on. In North America, most cases-about 70 percent are 1a or 1b subtypes. The rest are 2, 3, and 4. Type 2 is common in Japan and in China. Type 3 predominates in Europe and the United Kingdom. Type 4 is common in the Middle East and central Africa. Type 5 is rare in North America, but dominates in South Africa. Type 6 is often found in Hong Kong and Macao. Types 1a and 1b seem to cause the most severe disease, and the cases most resistant to treatment. In addition to these genotypes, there are many small variants of the genomes within the genotypes, forms that may multiply over time within the same individual and may also contribute to resistance to drugs.

This kind of genotyping is a research tool, and at least for the moment, has very little clinical significance. Type 1 is more resistant to treatment. but in fact you probably can’t even find out what genotype of virus you have unless you are in an experimental protocol at a research institution. The genotype or subtype of your HCV infection will probably make little difference in your treatment regimen.

While the virus was isolated in 1989, not until quite recently was it shown that it alone can cause the disease.This required making a tissue culture of the virus, making sure that the organism was purified, and that it was this organism that was causing HCV disease. This is an essential step in finding a treatment.

By 1992, effective methods for detecting HCV in the blood had been developed, and now blood is routinely screened for HCV. Although the risk of getting HCV from a blood transfusion is not zero, it’s pretty close: since 1994 the risk for transfusion-transmitted HCV infection has been so low that the CDC has been unable to detect a single case. But people who received transfusions before 1992 are at risk for HCV. And, as we will see later, they may have it without even knowing.

Today, 60 percent of the transmission of HCV can be traced to injection drug use, and, for reasons that are not entirely clear, the dramatic decrease in new cases of HCV began with decreases in new cases among this population. The decline accelerated considerably when blood screening for HCV began in 1992.

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