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-alpha 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.
BACKGROUND: Plasma levels of several chemokines and cytokines were evaluated in a cohort of 161 human immunodeficiency virus (HIV)positivepatients 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-alpha 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, coinfectedpatients 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.
Authors: Jason T Blackard; Gang Ma; Jeffrey A Welge; Lynn E Taylor; Kenneth H Mayer; Robert S Klein; David D Celentano; Jack D Sobel; Denise J Jamieson; Caroline C King Journal: J Med Virol Date: 2017-08-28 Impact factor: 2.327