Background: The host factors influencing the susceptibility to and the severity of tick-borne encephalitis (TBE) are poorly defined. The loss-of-function mutation in the chemokine receptor gene was identified as a risk factor for West Nile encephalitis and possibly for TBE, suggesting a protective role of CCR5 in encephalitis.
Methods: We studied the 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%) heterozygotes and 3 (1.5%) homozygotes in the TBE group, with no statistically significant difference in comparison with the controls. The 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 () and genotype patients. The TBE clinical presentation and CSF parameters in three homozygotes were unremarkable.
Conclusions: The lack of association of 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.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8955457 | PMC |
http://dx.doi.org/10.3390/pathogens11030318 | DOI Listing |
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