Grygorczuk et al.
The lack of the association of the CCR5 genotype with the clinical presentation and frequency of tick-borne encephalitis in the Polish population
Pathogens. 2022;11(3):318. doi: 10.3390/pathogens11030318
Host factors contributing to the susceptibility and severity of TBE are poorly defined. Chemokines (a family of small cytokines) interact with specific receptors which are selectively expressed on different leukocyte populations, and the changeable pattern of the chemokine ligand and leukocyte populations allows for the differential control of leukocyte migration and inflammatory infiltrate as well as the local immune response.
CCR5 is a receptor for the chemokines CCL3, CCL4, and CCL5 and is expressed on T-lymphocytes. CCR5 is a co-receptor for HIV-1 and antiretroviral drugs. In viral encephalitis, it may be involved in the lymphocyte migration into the cerebrospinal fluid. In TBE, the activated intrathecal T-lymphocytes are enriched in CCR5-positive cells. Mice unable to express CCR5 have unfavorable alterations of intrathecal response to several flaviviruses. In humans, this condition may be mimicked by ∆32 deletions of the CCR5 gene. The CCR5∆32 homozygosity correlates with an increased risk of fatal outcome of West Nile virus infections.
A Polish group has evaluated the clinical presentation of TBE in 39 patients in northeastern Poland – 36 heterozygous and 3 homozygous – for the CCR5∆32 mutation and in a control group of 205 patients.
The CCR5∆32 mutation did not associate with the clinical presentation or severity of TBE, and the authors concluded that CCR5 is not essential in preventing symptomatic disease and CNS involvement in TBE and that it does not play a decisive role in the primary infection or during the viremic phase.