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Original Article
Volume 345:707-714 September 6, 2001 Number 10
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Effect of Coinfection with GB Virus C on Survival among Patients with HIV Infection
Jinhua Xiang, M.D., Sabina Wunschmann, Ph.D., Daniel J. Diekema, M.D., Donna Klinzman, B.A., Kevin D. Patrick, M.A., Sarah L. George, M.D., and Jack T. Stapleton, M.D.

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ABSTRACT

Background Previous studies have suggested that people with human immunodeficiency virus (HIV) infection who are coinfected with GB virus C (GBV-C, or hepatitis G virus) have delayed progression of HIV disease. GBV-C is related to hepatitis C virus but does not appear to cause liver disease.

Methods We examined the effect of coinfection with GBV-C on the survival of patients with HIV infection. We also evaluated cultures of peripheral-blood mononuclear cells infected with both viruses to determine whether GBV-C infection alters replication in vitro.

Results Of 362 HIV-infected patients, 144 (39.8 percent) had GBV-C viremia in two tests. Forty-one of the patients with GBV-C viremia (28.5 percent) died during the follow-up period, as compared with 123 of the 218 patients who tested negative for GBV-C RNA (56.4 percent; P<0.001). The mean duration of follow-up for the entire cohort was 4.1 years. In a Cox regression analysis adjusted for HIV treatment, base-line CD4+ T-cell count, age, sex, race, and mode of transmission of HIV, the mortality rate among the 218 HIV-infected patients without GBV-C coinfection was significantly higher than that among the 144 patients with GBV-C coinfection (relative risk, 3.7; 95 percent confidence interval, 2.5 to 5.4). HIV replication, as measured by the detection of p24 antigen in culture supernatants, was reproducibly inhibited in cultures of peripheral-blood mononuclear cells by GBV-C coinfection. Coinfection did not alter the surface expression of HIV cellular receptors on peripheral-blood mononuclear cells, as determined by flow cytometry.

Conclusions GBV-C infection is common in people with HIV infection and is associated with significantly improved survival.


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From the Departments of Internal Medicine and Research, Iowa City Veterans Affairs Medical Center, and the University of Iowa College of Medicine (J.X., S.W., D.J.D., D.K., K.D.P., S.L.G., J.T.S.), and the Helen C. Levitt Center for Viral Pathogenesis and Disease (J.T.S.) — all in Iowa City, Iowa.

Address reprint requests to Dr. Stapleton at the Department of Internal Medicine, SW 54, GH UIHC, 200 Hawkins Dr., University of Iowa, Iowa City, IA 52242, or at jack-stapleton{at}uiowa.edu.

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