Background: Previous studies have suggested that people with human immunode
ficiency virus (HIV) infection who are coinfected with GB virus C (GBV-C, o
r hepatitis G virus) have delayed progression of HIV disease. GBV-C is rela
ted 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 o
f patients with HIV infection. We also evaluated cultures of peripheral-blo
od 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 duratio
n of follow-up for the entire cohort was 4.1 years. In a Cox regression ana
lysis adjusted for HIV treatment, base-line CD4+ T-cell count, age, sex, ra
ce, and mode of transmission of HIV, the mortality rate among the 218 HIV-i
nfected patients without GBV-C coinfection was significantly higher than th
at among the 144 patients with GBV-C coinfection (relative risk, 3.7; 95 pe
rcent confidence interval, 2.5 to 5.4). HIV replication, as measured by the
detection of p24 antigen in culture supernatants, was reproducibly inhibit
ed 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.