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Vol 53(2019) N 3 p. 342-345; DOI 10.1134/S0026893319020031 Full Text

A.V. Barkhash1*, I.V. Kozlova2, L.L. Pozdnyakova3, N.S. Yudin1, M.I. Voevoda1, A.G. Romaschenko1

New Genetic Marker of Human Predisposition to Severe Forms of Tick-Borne Encephalitis

1Federal Research Center Institute of Cytology and Genetics, Siberian Branch, Russian Academy of Sciences, Novosibirsk, 630090 Russia
2Scientific Centre for Family Health and Human Reproduction Problems, Irkutsk, 664003 Russia
3City Infectious Clinical Hospital No. 1, Novosibirsk, 630099 Russia

*barkhash@bionet.nsc.ru
Received - 2018-10-03; Revised - 2018-11-12; Accepted - 2018-11-14

The causative agent of tick-borne encephalitis (a neurotropic RNA virus from the Flavivirus genus) can cause both severe paralytic forms of the disease (meningoencephalitis, etc.) and milder nonparalytic forms (fever and meningitis). The organism response to viral infection (and, as a consequence, the nature and outcome of the disease) significantly depends on individual peculiarities of the human organism protective systems predetermined by genome structure. Human genetic predisposition to tick-borne encephalitis has been poorly studied. In the present work, the results of the search for new genes that predetermine the peculiarities and outcome of tick-borne encephalitis in humans are presented. The aim of the work was to verify the association between three previously detected (using the exome sequencing on a limited sample of tick-borne encephalitis patients with severe forms) SNPs: intronic rs3109675 (C/T) in the COL5A1 gene, intronic rs41554313 (A/G) in the POLRMT gene, and intergenic rs10006630 (C/A), and the predisposition to tick-borne encephalitis in a Russian population (using an extended sample of patients with different forms of tick-borne encephalitis). The association of the rs10006630 SNP located in chromosome 4 between the FABP2 and LINC01061 genes with a predisposition to tick-borne encephalitis was confirmed. This SNP can be considered as a new genetic marker of a human predisposition to severe forms of tick-borne encephalitis. The possible regulatory role of this SNP in the functioning of neighboring genes and a mechanism of its effect on the development of predisposition to severe forms of tick-borne encephalitis require further study.

tick-borne encephalitis, genetic predisposition, single nucleotide polymorphism



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