Virus May Slow Down AIDS


HANNOVER, Germany-New research published in the New England Journal of Medicine suggests the GB virus C may slow down the progression of human immunodeficiency virus (HIV), which causes AIDS.

The GB virus C, also known as hepatitis G, appears to be benign in nature. Researchers believe it does not cause inflammation of the liver or any chronic disease, as its secondary name would allude. It was named hepatitis G after being identified in the 1990s because it was thought to be the next virus in the hepatitis family.

The virus, which is transmitted by infected blood and sexual intercourse is reportedly carried by 2% of volunteer blood donors, leading researchers to believe more than 10 million people worldwide may carry the virus.

In one study, German researchers followed 200 HIV patients in Hannover. Within this group, 17% were also infected with GB virus C viremia, meaning the pathogen was detectable in the bloodstream, while 57% of the group had antibodies developed to fight the virus, suggesting they had been previously infected and fought of the pathogen. The remaining participants in the study did not have any evidence of previous or current GB virus C infections.

The research showed the greater amount of GB virus C found in an HIV patient's bloodstream, the fewer HIV viral cells present. While scientists do not understand this relationship, they are theorizing that the virus could be pushing the immune system to fight HIV, it could be directly killing HIV, or it could be a fluke in research.

The Hannover study showed that 4% of the patients with viremia died compared to 30% of those with antibodies and 40% of those with no traces of the GB virus C.

In a different study conducted in Iowa, 360 HIV patients were followed and tested for the GB virus C. During a four-year follow-up, 29% of participants carrying both viruses died in comparison to 56% of those participants with solely HIV.

For more information about GB virus C, long onto Johns Hopkins University's information page:

Information from www.sfgate,, the Associated Press

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