Background. Plasma levels of several chemokines and cytokines were evaluated in a cohort of 161 human immunodeficiency virus (HIV) - positive patients to shed light on a clinically relevant mechanism that would explain the putative beneficial effect of GB virus type C (GBV-C) coinfection. Methods. Markers for GBV-C infection were assessed in plasma samples. The syncitium-inducing ( SI) capacity of isolated virus from each patient was determined in MT-2 cells. Plasma cytokine and chemokine levels were quantified with use of a commercial enzyme-linked immunosorbent assay. Results. GBV-C viremia was found in 44 (27%) of 161 patients, and anti-E2 antibodies were found in 18 (21%) of 87. In contrast to the findings of ex vivo analysis, no statistically significant differences were observed in levels of CCL5, stromal cell - derived factor 1, interleukin-7, and tumor necrosis factor - a in plasma of patients with or without GBV-C viremia. Seventy-two (45%) and 89 (55%) of our patients harbored SI and non-SI (NSI) strains, respectively. GBV-C viremia was less prevalent among patients with SI strains ( 13 [18%] of 72) than among patients with NSI strains (30 [34%] of 89; P = .6). Of interest, coinfected patients with SI strains had significantly higher CD4(+) T cell values than did patients who were not coinfected. Conclusions. Our results suggest that GBV-C infection does not appear to influence the expression of the cytokines and chemokines analyzed herein in a clinically relevant context. Alternative explanations for the elevated levels of HIV-inhibitory chemokines are needed to explain the putative beneficial effect of GBV-C.