Virus Found to Extend Life for HIV Patients

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An apparently harmless and relatively common virus discovered only six years ago allows HIV-positive people to live substantially longer by slowing the progression to full-blown AIDS, researchers report today in two new studies.

The virus is called hepatitis G, but it doesn’t cause inflammation of the liver or any other illness that researchers have discovered. It does, however, cut the death rate from AIDS by almost 50%, two teams report in today’s New England Journal of Medicine. That is a surprising finding because other hepatitis viruses accelerate progression of HIV.

“This leads us to believe [the virus] is one factor explaining how some people live longer and more healthily with their HIV infection than other HIV-infected people do,” said Dr. Jack Stapleton of the Iowa College of Medicine, one of the authors of the study.


Experts such as Dr. Steven Wolinsky of Northwestern University Medical School held out hope that the discovery could lead to new ways to treat HIV infections, perhaps by mimicking the activity of the virus if researchers can find out how it works.

Nonetheless, Wolinsky cautioned in a editorial, “there are many questions that remain to be answered.” Most notably, researchers currently do not know how the virus works to inhibit AIDS, although some of the new research points to clues.

The finding also comes along with a warning: Doctors worry that some HIV-positive people may be tempted to infect themselves with the virus, which is also known as GBV-C, hoping to prevent the onset of AIDS. They caution against that because so little is known about the virus.

Ultimately, however, researchers may want to do just that, said Dr. Isa K. Mushahwar of Abbott Laboratories in North Chicago, who was one of the first to discover the new virus.

“It’s very exciting now that it is confirmed statistically that infection by GBV-C prolongs life,” Mushahwar said. “Since it has now been proven that GBV-C infection is not harmful . . . the ethical question becomes, should we infect the HIV-positive?”

Any attempt to do so will require many more studies, the involvement of the federal Food and Drug Administration and other complications, he conceded.


“But if it helps and prolongs life . . . the question becomes, why not?”

The hepatitis G virus is a curious beast that has been under scientists’ noses for at least half a century. Because it does not produce any known symptoms, it had largely been ignored.

The discovery of its effect on AIDS came about largely by accident. Stapleton and his colleagues were actually studying the effect of alcohol and conventional hepatitis viruses on HIV progression and stumbled across the relationship to hepatitis G.

The virus is found in about 1% to 2% of healthy blood donors in the U.S. Because the virus is transmitted by body fluids and infected needles, just like HIV, it is far more common among people who are HIV-positive; as many as 40% of them carry the hepatitis G virus.

The virus was first identified in 1995 by two teams of scientists--one from Abbott Laboratories in North Chicago and one from Genelabs Technologies in Redwood City. They took advantage of modern, highly sophisticated molecular biology techniques to do so.

Mushahwar and the Abbott team used frozen blood samples from a Chicago surgeon named George Baker who developed hepatitis in the early 1960s. Virologist Jungsuh P. Kim at Genelabs used a blood sample from another patient with a mysterious case of hepatitis.

Both identified the same virus. The Abbott team called the new virus GB virus C (GBV-C) because it was similar to the hepatitis C virus, while Kim called it hepatitis G. Although both names are now used, GBV-C is becoming more common because the virus does not seem to infect the liver or cause any other symptoms in humans. Baker’s hepatitis was caused by a different virus also present in his body.


GBV-C is a virus whose structure is similar to those that cause hepatitis C, yellow fever and dengue.

In 1998, Dr. Michael P. Manns and his colleagues at Medical School Hanover in Germany compared HIV-positive individuals who were also infected with GBV-C to a group of HIV-positive people who did not have the hepatitis G virus. Those who had the virus had higher levels of CD-4 cells, a key diagnostic indicator for AIDS. At least 10 other groups have now replicated that finding.

The new studies go beyond that previous research and demonstrate that having a hepatitis G infection translates into a longer life span.

Their study group included 362 HIV-positive individuals, 144 (39.7%) of whom were also infected by GBV-C. Over the four years of follow-up in the study, about 29% of the patients infected with GBV-C died, compared with 56% of those who were not infected.

When they took other infections and risk factors into account, the Iowa team concluded that those who were not infected with GBV-C were 3.68 times as likely to die of AIDS as those with the virus.

That’s “very exciting . . . because it may lead us to other treatments or other approaches to treatment,” said Dr. Daniel Diekema, one of the researchers.


In the second report, Dr. Hans L. Tillman, Manns and their colleagues studied 197 HIV-positive patients. Their results were similar to the Iowa team’s.

In the second phase of the Iowa study, Dr. Jinhua Xiang and virologist Sabina Wunschman of the Stapleton team grew HIV in white blood cells in a laboratory dish. They found that if the cells were infected with GBV-C about 24 hours before the HIV infection, replication of HIV was reduced by 30% to 40%.

The virus was less effective at blocking replication if it was introduced at the same time as HIV or after the infection was established.