RESUMO
Respiratory syncytial virus (RSV) can inhibit the proliferative response of human peripheral blood mononuclear cells (PBMC) in vitro. This inhibition is mediated by an extracellular RSV-induced factor. In the present study, the factor was clearly identified as interferon (IFN)-alpha. The RSV-induced IFN-alpha bound strongly to PBMC and inhibited the anti-RSV proliferative response only when added within the first few days of stimulation. There was, however, no concomitant decrease in the production of interleukin (IL)-2 nor in the cell surface expression of CD25, CD71, and HLA-DR. Inhibition by RSV-induced IFN-alpha was unrelated to the levels of IL-1, -2, and -6 or of IFN-gamma induced by RSV in vitro or to the presence of IL-1 inhibitor, tumor necrosis factor-alpha, prostaglandin, or IL-10. Immunosuppression by IFN-alpha may significantly affect the outcome of infection and reinfection with RSV.
Assuntos
Antivirais/metabolismo , Tolerância Imunológica/fisiologia , Interferon-alfa/metabolismo , Leucócitos Mononucleares/metabolismo , Vírus Sinciciais Respiratórios/efeitos dos fármacos , Antivirais/isolamento & purificação , Antivirais/farmacologia , Células Cultivadas , Citocinas/análise , Relação Dose-Resposta a Droga , Humanos , Interferon-alfa/isolamento & purificação , Interferon-alfa/farmacologia , Ativação Linfocitária/efeitos dos fármacos , Linfócitos T/efeitos dos fármacos , Fator de Necrose Tumoral alfa/biossínteseRESUMO
The effect of respiratory syncytial virus (RSV) on the cellular immune response of human mononuclear cells in vitro was examined. Inhibition by RSV of the lymphocyte response to phytohemagglutinin in vitro was confirmed using cells from human umbilical cord blood. In addition, RSV significantly inhibited both the proliferative and T cell colony responses of human mononuclear cells to Epstein-Barr virus. An RSV-specific cellular immune response was induced in vitro by stimulation of mononuclear cells from RSV-seropositive donors with beta-propiolactone-inactivated RSV. This RSV-specific response was significantly inhibited by infectious RSV itself, and the inhibition was mediated by an extracellular factor produced by RSV-infected mononuclear cells. A similar inhibition in vivo of the RSV-induced cellular immune response may contribute significantly to delayed recovery from primary infection and to reduced resistance to subsequent infections.
