Abstract
BACKGROUND: The host factors influencing the susceptibility to and the severity of tick-borne encephalitis (TBE) are poorly defined. The loss-of-function Δ32 mutation in the chemokine receptor gene CCR5 was identified as a risk factor for West Nile encephalitis and possibly for TBE, suggesting a protective role of CCR5 in Flavivirus encephalitis. METHODS: We studied the CCR5 genotype in 205 TBE patients stratified by a clinical presentation and 257 controls from the same endemic area (Podlasie, Poland). The genotype distribution between the groups and differences between TBE patients with different genotypes were analyzed. RESULTS: There were 36 (17.6%) CCR5Δ32 heterozygotes and 3 (1.5%) homozygotes in the TBE group, with no statistically significant difference in comparison with the controls. The CCR5Δ32 allele did not associate with the clinical presentation or the severity of TBE. The cerebrospinal fluid (CSF) inflammatory parameters did not differ between the wild-type (wt/wt) and wt/Δ32 genotype patients. The TBE clinical presentation and CSF parameters in three Δ32/Δ32 homozygotes were unremarkable. CONCLUSIONS: The lack of association of CCR5Δ32 with the risk and clinical presentation of TBE challenges the suspected CCR5 protective role. CCR5 is not indispensable for the effective immune response against the TBE virus.