CYTOKINES AND ANTIBODIES IN EXPERIMENTAL INFECTION OF WILD AND LABORATORY RODENTS (RODENTIA) WITH TICK-BORNE ENCEPHALITIS VIRUS

Autor: V. N. Bakhvalova, V. V. Panov, O. F. Potapova, O. V. Morozova
Jazyk: English<br />Russian
Rok vydání: 2017
Předmět:
Zdroj: Вопросы вирусологии, Vol 62, Iss 4, Pp 186-192 (2017)
Druh dokumentu: article
ISSN: 0507-4088
2411-2097
DOI: 10.18821/0507-4088-2017-62-4-186-192
Popis: Persistence modeling was performed by means of infection of the wild rodents: northern red-backed vole Myodes rutilus (Pallas, 1779) and striped field mouse Apodemus agrarius (Pallas, 1771), as well as of laboratory mice with the tick-borne encephalitis virus (TBEV) in tick suspensions with subsequent detection of the TBEV, hemagglutination inhibition and virus-neutralizing antibodies, as well as expression of cytokine genes during 4 months. Detection rate of the TBEV RNA and antigen E remained high during the whole period of observations; however, virus pathogenic for laboratory suckling mice was isolated mainly during a period of 8 days post infection. At the late stages of the persistent infection (1-4 months) the TBEV RNA detection rate in northern red-backed voles and laboratory mice remained high, whereas in striped field mice it significantly declined (p < 0.001). The viral loads were significantly higher (p < 0.001) in the wild rodents compared to the laboratory mice. Average frequencies of Th2 cytokine gene expression were similar for M. rutilus (50.0 ± 8.5%) and A. agrarius (50.0 ± 9.6%) during the whole period, but Th1 cytokine mRNA detection rate after transcription activation in 2 days post infection and subsequent return to the original values were different (22.2 ± 5.0% and 38.1 ± 7.6%, respectively (p > 0.05)). Meanwhile, a part of animals with interleukin 1β mRNA was significantly higher among A. agrarius than among M. rutilus (p < 0.05), which might cause low levels of spontaneous TBEV infection of field mice compared to red voles. Hemagglutination inhibition and virus-neutralizing antibodies were revealed in wild rodents in 30 days post infection and remained at detectable levels during 4 months. Thus, the TBEV persistence in small rodents was accompanied by the detection of the pathogenic virus in the early period, the viral RNA and antigen E during 4 months with high viral loads in wild animals exceeding the values in laboratory mice. Changes in the proinflammatory cytokine gene expression frequencies and the TBEV-specific antibodies pointed at immunomodulation as the possible mechanism of the TBEV persistence.
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