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Review
. 2004 Sep;42(9):3915-9.
doi: 10.1128/JCM.42.9.3915-3919.2004.

GB virus type C: a beneficial infection?

Jack T Stapleton  1 , Carolyn F Williams, Jinhua Xiang
Affiliations
Review

GB virus type C: a beneficial infection?

Jack T Stapleton et al. J Clin Microbiol. 2004 Sep.
No abstract available

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Figures

FIG. 1.
FIG. 1.
The GBV-C genome is composed of a single-stranded, positive-polarity RNA molecule that encodes a long polyprotein. A nontranslated region at the 5′ end of the open reading frame (5′ntr) contains an internal ribosomal entry site, and there is another nontranslated region at the 3′ end of the genome (3′ntr). It is believed that the predicted viral envelope proteins (E1 and E2) are cleaved by cellular proteases but that the nonstructural proteins NS2, NS3, NS4A (*4A), NS4B (*4B), NS5A, and NS5B are cleaved by the viral protease (NS3) in reactions involving a protease cofactor (NS4A). The coding region for the nucleocapsid protein has not yet been identified.
FIG. 2.
FIG. 2.
Comparison of the relative impacts of different predictors of HIV disease progression. Different mortality indexes of death for persons with HIV are compared for those persons with and without GBV-C, those persons with and without the protective CCR5 allele, and by stage of HIV disease, CD4 cell counts, and HIV RNA levels. An index value of greater than 1 indicates a higher risk of death, and an index value of less than 1 demonstrates a protective effect. As described in the text, men who were GBV-C RNA positive at both the early and late visits (+ +) were more than twice as likely to survive compared to those who were GBV-C RNA negative on both visits (− −) (index = 0.41), whereas those who cleared viremia between visits were more than twice as likely to die (index = 2.39). By comparison, those heterozygous for the CCR5 HIV coreceptor gene (Δ32) were also protected from death, but this protection was less than that seen for individuals with persistent GBV-C infection (index = 0.63). Another way to conceptualize the magnitude of this protection is to note that it is as large as the difference between a patient having a CD4 cell count of 500 to 750 (*high) and a patient with only a mid-range CD4 count (mid; 200 to 350 cells; mortality index = 0.47). Conversely, the negative impact of losing GBV-C infection is the same as the risk of death among persons with mid-range CD4 cell counts compared to those with high CD4 cell counts (index = 2.1). It is of note that while these protective effects are strong, HIV viral load (HIV RNA) is one of the strongest predictors of survival and that when those with low (3,000 to 10,000 [3-10 K] genome equivalents per milliliter) versus high (>100,000) viral loads are compared, the effect is considerably greater than that of the presence of GBV-C or CCR5 polymorphisms or a high versus a moderate CD4 count. wt, wild type.
FIG. 3.
FIG. 3.
Potential effects of GBV-C that may alter HIV disease. GBV-C must interact with a receptor (or receptors) on lymphocytes to initiate infection. (Bottom) GBV-C replication (i) increases chemokine expression and down-regulates the expression of CCR5 (13) and (ii) alters Th cytokines in vitro (; J. Xiang et al., Prog. Abstr. 10th Conf. Retrovir. Opportun. Infect., abstr. 156), both of which lead to decreased HIV replication. Similarly, GBV-C viremia is associated with decreased CCR5 expression and a modulation of Th cytokines in clinical studies (5, 6). These effects may be mediated by the GBV-C E2 protein via interactions with CD81 on the surfaces of CD4 cells (5). In addition to the effects of GBV-C on chemokine and cytokine expression, other undefined effects of GBV-C may also influence HIV disease progression.
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