Role of the genetic variant CCR5032 in HBV infection and HBV/HIV co-infection

CCR5 is a chemokine receptor that mediates the action of inflammatory cells, besides acting as an HIV coreceptor. CCR5 Delta 32 states for a genetic variant containing a 32 base pair deletion in the coding region of the CCR5 gene. In homozygosis, CCR5 Delta 32 results in the lack of CCR5 expression on the cell surface, which was associated with protection against HIV infection. Heterozygous individuals for CCR5 Delta 32 have a reduced CCR5 expression. Recent evidence demonstrates that CCR5 and CCR5 Delta 32 are involved in the pathogenesis of other viral infections besides HIV infection. Nevertheless, the role of CCR5 and CCR5 Delta 32 in HBV infection is not clear and conflicting results have been reported. Thus, the objective of this study was to investigate the role of CCR5 Delta 32 in HBV mono-infection and HBV/HIV co-infection in a population from southern Brazil. A total of 1113 individuals were evaluated, divided in controls (n = 334), HBV + (n = 335), HBV + /HIV + (n = 144), and including an HIV + group to complement the analyses (n = 300, obtained from a previous study of our research team). The CCR5 Delta 32 allele frequencies found were 7.5 %, 9.0 %, and 3.1 %, respectively for controls, HBV +, and HBV + /HIV + patients. The individuals were classified in CCR5 Delta 32 allele carriers and CCR5 Delta 32 allele non-carriers and the groups were compared using binary logistic regression adjusted for covariates. No significant effect of the CCR5 Delta 32 variant was observed on the susceptibility or protection against HBV monoinfection in individuals from southern Brazil. A potential protective effect of CCR5 Delta 32 on HBV/HIV co-infection was observed. However, it can be due to the effect of CCR5 Delta 32 in the protection against HIV infection or external factors not covered in the study. Finally, this study contributes to the understanding of the role of CCR5 in HBV infection, suggesting no effect of CCR5 Delta 32 on susceptibility to HBV mono-infection.