INBIRS   24491
INSTITUTO DE INVESTIGACIONES BIOMEDICAS EN RETROVIRUS Y SIDA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
CD4+ T cells are permissive to Respiratory Syncytial virus infection
Autor/es:
J. PANDOLFI; S. RAIDEN; I. SANANEZ; G. ERNST; C. JANCIC; A. CEBALLOS; J. GEFFNER; L. ARRUVITO
Lugar:
Buenos Aires
Reunión:
Congreso; Reunion Anual SAI; 2015
Institución organizadora:
Sociedad Argentina de Inmunología
Resumen:
Abstract: Background: Respiratory Syncytial virus (RSV) is the leading cause of severe bronchiolitis in young infants. We have recently reported that RSV infection induces a dramatic reduction in the frequency of peripheral blood Tregs in children. Although human airway epithelial cells are the main target of RSV, it has been shown that the virus can also infect immune cells as DCs. However, no studies have evaluated whether CD4+T cells are permissive to RSV infection.Aims: 1) to test the in vitro susceptibility of cord blood CD4+T cells to RSV infection; 2) to determine if RSV infection modulates the function of CD4+T cells; 3) to investigate whether RSV proteins are detected in peripheral blood CD4+T cells of infected infants.Results: We found that cord blood CD4+T cells exposed to RSV or co-cultured with infected bronchial epithelial cells were effectively infected by RSV, as indicated by the expression of viral proteins and mRNA. RSV infection of CD4+T cells inhibits IL-2 production and cell proliferation induced by different stimuli (p<0.01). We detected RSV proteins in CD4+T cells from severe infected children by flow cytometry (n=12). Moreover, we found that the percentage of RSV+CD4+T cells negatively correlated (r= -0.72, p<0.01) with CD4+T cell frequency in peripheral blood.Conclusions: We show that CD4+T cells from cord blood are permissive to RSV infection, and also that it modulates cell function. Moreover we found that CD4+T cells from severe infected infants express viral antigens. Our finding could partially explain why RSV infection fails to induce long lasting immunity.