GB individuals virus C replication in cerebrospinal fluid of HIV positive

Background GB virus C (GBV-C) is an orphan Flavivirus distantly related to hepatitis C virus (HCV). GBV-C infection in humans is common and its transmission is similar to both HCV and HIV, including sexual, parenteral and vertical transmission. The aim of this study was to investigate the presence and compartimentalization of GBV-C strains in plasma, PBMC and cerebrospinal fluid (CSF) of HIV positive patients in an attempt to identify GBV-C replication in CSF. Methods This retrospective study involved 22 HIV positive patients who underwent a lumbar puncture for diagnostic purposes. To evaluate the prevalence of GBV-C infection in our Centre, a control group of 150 HIV positive patients was included in the study. GBV-C-RNA was searched for in paired plasma, CSF and PBMC by means of nested PCR for 5’UTR. GBV-C genotype was identified by direct sequencing and phylogenetical analysis. GBV-C population in plasma and CSF was characterized by analysis of at least 25 clones for each compartment. HIV load was measured by a quantitative PCR (Amplicor HIV Monitor). Results GBV-C-RNA was detected in plasma from 37/150 (25%) control patients and in the PBMC from 3/34 (9%) patients with GBV-C detected in plasma. GBV-C-RNA was identified in 5/22 (23%) plasma, in none of PBMC and in 2/5 (40%) CSF samples obtained from the 5 GBV-C positive patients in plasma. This data showed that the presence of GBV-C-RNA in plasma was similar in control group and study population. Albeit GBV-C-RNA was detected in 3 PBMC of control group and in none PBMC of the study population, the difference was not statistically significant. Direct sequencing of GBV-C 5’UTR detected in plasma revealed the presence of genotype 2 in three patients GBV-C-RNA negative in CSF. Analysis of GBV-C population within the 5’UTR showed the presence of GBV-C genotype 2 in plasma and genotype 3 in CSF of one patient, whereas the other case had mixed infection in plasma (genotype 3/1) and genotype 3 alone in CSF. Plasma HIV-RNA levels were significantly higher in patients with CSF positive for GBV-C than in those with GBV-C negative CSF (mean values 5.35 vs 4.39 Log copies/ml, p=0.027). HIV viral load in CSF was similar in all patients (mean values 3.66 vs 3.14 Log copies/ml). Conclusion These findings suggest the replication of GBV-C in CSF and the selection of genotype 3 in this compartment. The presence of discordant genotypes in paired plasma/CSF of one patient could be due to a past mixed infection in plasma.