Enterovirus receptors and virus replication in human leukocytes

T Vuorinen, R Vainionpaa, J Heino and T Hyypia Department of Virology, University of Turku, Finland. tytti.vuorinen@utu.fi Although enteroviruses cause a great variety of diseases including meningitis, paralysis and myocarditis, the life-cycle of these viruses in man is still quite poorly understood...

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Veröffentlicht in:Journal of general virology 1999-04, Vol.80 (4), p.921-927
Hauptverfasser: Vuorinen, T, Vainionpaa, R, Heino, J, Hyypia, T
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Sprache:eng
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Zusammenfassung:T Vuorinen, R Vainionpaa, J Heino and T Hyypia Department of Virology, University of Turku, Finland. tytti.vuorinen@utu.fi Although enteroviruses cause a great variety of diseases including meningitis, paralysis and myocarditis, the life-cycle of these viruses in man is still quite poorly understood. The role of human leukocytes as a target for enterovirus infections was studied in this report. Despite great similarity in the structure and replication of coxsackievirus B3 (CBV3), echovirus 1 (EV1), and poliovirus 1 (PV1), the ability of these viruses to infect human peripheral blood mononuclear cells (PBMC), and B (Raji), T (Molt-4) and monocytic (U- 937) cell lines differed markedly. CBV3 attached both to PBMC and the three haematopoietic cell lines studied, whereas EV1 bound only to PBMC. Generally, the attachment of PV1 was very poor. The binding assays mostly correlated with the expression of CD55 (decay accelerating factor, DAF) and alpha2beta1-integrin (VLA-2), which are known to act as receptors for CBV3 and EV1, respectively, as well as with the expression of the PV receptor on the cell surface. To analyse virus replication in the cells, viral protein and nucleic acid syntheses were studied by immunoprecipitation and RT-PCR. CBV3 was able to replicate in Raji and Molt-4 cells, even though no expression of DAF was detected, whereas in the monocytic cell line, viral protein synthesis was detected only after transfection of virus RNA. Neither CBV3 nor EV1 replicated in PBMC and all haematopoietic cells studied seemed to be poorly permissive for PV1 replication.
ISSN:0022-1317
1465-2099
DOI:10.1099/0022-1317-80-4-921