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Background: The host factors influencing the susceptibility to and the severity of tick-borne encephalitis (TBE) are poorly defined. The loss-of-function <i>Δ32</i> mutation in the chemokine receptor gene <i>CCR5</i> was identified as a risk factor for West Nile encephalitis and possibly for TBE, suggesting a protective role of CCR5 in <i>Flavivirus</i> encephalitis. Methods: We studied the <i>CCR5</i> 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%) <i>CCR5</i><i>Δ32</i> heterozygotes and 3 (1.5%) homozygotes in the TBE group, with no statistically significant difference in comparison with the controls. The <i>CCR5</i><i>Δ32</i> 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 (<i>wt/wt</i>) and <i>wt/</i><i>Δ32</i> genotype patients. The TBE clinical presentation and CSF parameters in three <i>Δ32/</i><i>Δ32</i> homozygotes were unremarkable. Conclusions: The lack of association of <i>CCR5</i><i>Δ32</i> 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.