Background: It has recently been reported that GB Virus type C (GBV-C) can decrease HIV-1 replication of R5 and X4 variants and alter beta-chemokine expression pattern ex  vivo, suggesting a possible mechanism of GBV-C interference with HIV replication. We therefore evaluated plasma levels of several chemokines and cytokines in a cohort of 161 HIV⁺ patients patients to shed light into a clinically relevant mechanism that would explain the beneficial effect of GBV-C co-infection.

Methods: Markers for GBV-C infection (viremia: GBV-C RNA; resolved infection: anti-E2 antibodies) were assessed in plasma samples from 161 HIV-1-infected patients. The syncitium-inducing capacity was determined in MT-2 cells for each patient. Plasma cytokine and chemokine levels were detected by commercial ELISA.

Results: GBV-C viremia was found in 43/161 patients  (27%), and anti-E2 antibodies in 19/87 (21%); 72 (45%) and 89 (55%) patiens harbored syncitium-inducing and non-syncitium-inducing) strains, respectively. No epidemiological differences were observed between the syncitium-inducing and non-syncitium-inducing groups. GBV-C viremia tended to be less prevalent in syncitium-inducing patients than in non-syncitium-inducing (13/72, 18% vs. 30/89, 36%, respectively; p >0.05). No statistically significant differences were observed in the plasma levels (in pg/ml) of IL-7 (8.3±4.8; 9.7± 5.8), SDF-1 (387±275; 382±295), RANTES (30.918±23.418; 25.602±18.910) and TNF-a (3.5±4.2; 4.1±3.7) of patients with or without GBV-C viremia, respectively. Syncitium-inducing patients showed higher levels of IL-7 (13.1±5.7; 6.5±3.5, p = 0.005), RANTES (30.031±20.037; 24.292±19.898, p=0.035), TNF-a (6.6±4.7; 2.3±1.8, p = 0.000) and lower levels of SDF-1 (8.3±4.8; 9.7±5.8, p = 0.06), than non-syncitium-inducing patients, but they were not significantly altered by the concomitant infection with GBV-C, nor by the presence of anti-E2 antibodies.

Conclusions: GBV-C infection does not seem to significantly alter the chemokine/cytokine levels analyzed here in a clinically relevant context. Additional immunological and/or molecular factors might be involved in mediating the beneficial effects of GBV-C during the course of HIV infection.

Keywords: hepatitis G virus; chemokine; cytokine