GB Virus C and Mortality from HIV Infection

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Abstract
The reports of Xiang et al.1 and Tillmann et al.2 (Sept. 6 issue) further document that coinfection with the apparently nonpathogenic flavivirus GB virus C (GBV-C, or hepatitis G virus) prolongs survival in patients infected with the human immunodeficiency virus (HIV). As the accompanying editorial3 emphasizes, there are no causal inferences to be drawn from these observations, and the suggestion that therapy with GBV-C might improve survival among HIV-infected patients is correctly labeled as “premature.” Although viral cross-talk of this sort has been described in a number of other experimental systems,4 there are other possible explanations for the “protective” effect. For example, a potent cytotoxic-T-lymphocyte response to one viral infection may reduce the level of cytotoxic-T-lymphocyte activity directed to infection by a second virus.5 Persons who have a strong cytotoxic-T-lymphocyte response to HIV may have more difficulty mounting such a response to GBV-C and may thus be less likely to clear GBV-C infection. Tillmann et al. demonstrate no clear protective effect of exposure to GBV-C (as determined by a test for anti-E2 antibodies) but do demonstrate an obvious “protective” effect in those in whom GBV-C RNA was detected. Failure to clear active GBV-C infection may thus be an indirect marker of a particularly potent cytotoxic-T-lymphocyte response to HIV. This hypothesis, which can be readily tested, predicts that “therapeutic” coinfection with GBV-C would have no benefit for HIV-infected patients.

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