RESUMEN
The effect of a cationic ionophore, monensin, on the replication of Mayaro virus in monkey kidney TC7 and Aedes albopictus cells has been studied. Treatment of these cells with 1 micromol/l monensin during infection did not affect the virus protein synthesis but inhibited severely the virus replication. Electron microscopy of the cells infected with Mayaro virus and treated with monensin revealed that the morphogenesis of Mayaro virus was impaired in TC7 but not in A. albopictus cells.
Asunto(s)
Alphavirus/efectos de los fármacos , Monensina/farmacología , Proteínas Virales/efectos de los fármacos , Replicación Viral/efectos de los fármacos , Aedes/citología , Alphavirus/fisiología , Alphavirus/ultraestructura , Animales , Línea Celular , Células Clonales/microbiología , Haplorrinos , Riñón/citología , Proteínas Virales/biosíntesisRESUMEN
Infection of mice with Trypanosoma cruzi, the causative protozoan agent of human Chagas' disease, leads to immunosuppression of the T cell compartment and to chronic cardiac inflammation which resembles the human infection. Recently, reinduction of programmed cell death by apoptosis in mature T cells has been demonstrated. It has been suggested that mature T cell apoptosis could play a role in immunosuppression caused by virus infection. In this report, we have investigated the occurrence of mature T cell apoptosis in murine experimental Chagas' disease. Infection with T. cruzi metacyclic forms led to a relative accumulation of CD8 T cells over CD4 T cells in the spleens of infected mice. Splenic T cells from T. cruzi-infected donors, but not from control littermates, died in vitro upon stimulation with T cell mitogens Con A and anti-TCR-alpha beta mAb in a dose-dependent fashion. DNA fragmentation into nucleosome-sized bands was detected in the supernatants of CD4+ T cells from infected origin, after stimulation with the T cell mitogen Con A. Upon in vitro stimulation with either anti-TCR-alpha beta or Con A, CD4+ T cells were susceptible to elimination, whereas CD8+ T cells were not. Splenic T cells from infected donors were markedly unresponsive to anti-TCR mAb in proliferative assays and underwent apoptosis in vitro, as assessed by electron microscopy. Apoptosis also occurred in vivo in the course of acute infection, as seen by DNA fragmentation in freshly explanted splenic cells and purified T cell subsets. The data indicate that activation-induced CD4+ T cell death by apoptosis is a prominent feature of experimental infection with T. cruzi, and could play a role in immunosuppression and parasite persistence in infected hosts.
Asunto(s)
Apoptosis/inmunología , Linfocitos T CD4-Positivos/inmunología , Enfermedad de Chagas/inmunología , Animales , Complejo CD3/inmunología , Linfocitos T CD4-Positivos/ultraestructura , Linfocitos T CD8-positivos/inmunología , ADN/metabolismo , Masculino , Ratones , Ratones Endogámicos BALB C , Receptores de Antígenos de Linfocitos T alfa-beta/inmunología , Bazo/citologíaRESUMEN
Infection of HEp-2 cells by enteropathogenic Escherichia coli (EPEC) was examined by transmission and scanning electronmicroscopy. EPEC strains of serogroups O111:K58 and O55:K59 recently isolated from human patients did not exhibit enterotoxic activity, as judged by the Vero-cell and suckling-mouse assays, or invasive ability as judged by the Sereny test. These strains attached to and penetrated HEp-2 cells. Transmission electronmicroscopy showed bacteria in close contact with cell membranes 15 min after infection; later, intense swelling and budding of membranes and penetration of EPEC into the cell cytoplasm occurred. Intracellular bacteria were enclosed in membrane-bound vacuoles in the cell cytoplasm underlying localised adherence sites observed by light microscopy. Scanning electronmicroscopy showed morphologically altered membranes only at the sites of bacterial attachment. Bacteria inactivated by ultraviolet light were not internalised and cytochalasin B (greater than or equal to 10 mg/L) markedly inhibited uptake. These observations suggest that penetration of EPEC into HEp-2 cells occurs by an endocytic process in metabolically active bacteria.