AIDSWEEKLY Plus; August 12, 2002
Staff Medical Writer

Yet some people are resistant to infection: the reason for this is a mutation in their DNA that prevents HIV from invading certain immune cells and destroying them. BonnGermany scientists have now discoveredhoweverthat this resistance to HIV increases the probability of a persistent infection with hepatitis Ca disease that can also be fatal. The findings recently published in the journal Gastroenterology may influence possible therapeutic strategies for tackling HIV infections.

When a hepatitis C virus infects a liver cellthe cell secretes so-called chemokines into the blood. Chemokines are signal substances that normally attract inflammatory cells. These "T-lymphocytes" kill the infected cell and in doing so also kill the viruses that have caused the infection. T-lymphocytes have a sensor for chemokines on their surface.

Howeverthis sensor does not work in some humans: Due to a mutationtheir cells cannot express a functional sensor on the cell surface. Thusa liver cell's cry for help is not answered because the immune cells are blind and deaf to virus attacks. Therefore the body obviously finds it difficult to defend itself against other infections like hepatitis C.

Howeverthe same mutation also prevents this person from contracting HIV infections: AIDS virusesamong other thingsinfect T lymphocytesput them out of action and in doing so cause the fatal immune deficiency which gave the disease its name. Most HIV strains enter the cells using the chemokine sensor as a "gateway." If it is alteredthe virus cannot invade the immune cell.

Every cell has two copies of the sensor gene - one from the motherone from the father. In people who have one mutated copyHIV infection takes a less progressive course of disease. If both copies are mutatedthe person affected is resistant to most HIV strains.

About 1% of the German population has inherited two defective sensor genes. Among patients infected with the hepatitis C virus this percentage is markedly higher: "Twelve people out of 153 with hepatitis C antibodies had two copies of the mutated gene," Professor Ulrich Spengler from the Medical Clinic and Policlinic I explained. This is the equivalent to 7.8%which is much higher than would be statistically expected. "The amount of viruses found in these patients' blood was up to four times as high as with hepatitis C patients without this mutation."

The result indicates that the mutation facilitates to establish persistent infection by the viruses causing hepatitis. "A powerful immune response is especially important in the early phase of a hepatitis C infection," Spengler said. The more effective the immune system works in this "acute phase," the more likely it is that the body will cope with the virus attack. Otherwise there is a risk of the hepatitis becoming chronic. The after-effects of this can involve scarring of this vital organ.

The circulation of blood through a cirrhotic liver is sometimes so difficult thatfor examplethe blood vessels inside the esophagus may become pathologically distended and burst during food intake. Apart from that there is a substantially higher risk of liver cancer in patients with chronic hepatitis C ( Gastroenterology 2002 Jun;122(7):1721-8).

There are around 150 million hepatitis C patients worldwide. One in 200 Germans are infected with the dangerous virus. In three-quarters of those affected the disease becomes chronic - probably because their immune system was not sufficiently effective in the early phase. "We do not know what exactly determines whether the body's defense is successful," Spengler noted"howeverin some cases the mutation of the chemokine sensor gene seems to play an important part." Possible defense strategies against AIDS that are based on interfering with the chemokine sensors could therefore have drastic side effects - "a risk which definitely needs to be considered as part of further research."

This article was prepared by AIDS Weekly editors from staff and other reports.

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