Asunto(s)
Arenaviridae/crecimiento & desarrollo , Arenavirus del Nuevo Mundo/crecimiento & desarrollo , Encéfalo/microbiología , Fiebre Hemorrágica Americana/microbiología , Interferencia Viral , Animales , Células Cultivadas/microbiología , Inductores de Interferón/farmacología , Ratones , Replicación ViralAsunto(s)
Arbovirus/efectos de la radiación , Fiebres Hemorrágicas Virales/microbiología , Rayos Ultravioleta , Replicación Viral/efectos de la radiación , Arbovirus/efectos de los fármacos , Isótopos de Carbono , Citarabina/farmacología , ADN Viral/efectos de la radiación , ARN Viral/efectos de la radiación , Efectos de la Radiación , Replicación Viral/efectos de los fármacosRESUMEN
Supernatants from Vero cells persistently infected with Junin virus interfered with cytolitic and lethal activities of standard virus. Two Vero cell sublines, chronically infected with Junin virus named VRJ1 and VRJ3, were obtained after prolonged cultivation of cells which survived primary infection. VFJ1 was maintained over a period of 48 days, by biweekly serial transfers while VRJ3, similarly treated, was cultivated for 385 days. One of the characteristics of these cell lines was resistance against superinfection with homologous virus that ordinaily produced CPE and plaques in normal Vero cells; the cells were then considered chronically infected. Supernatants taken at different cell passage level were tested for its interference activity after centrifugation to eliminate floating cells and debris. The degree of CPE intensity caused by inoculation of Vero cells with 10(4), 10(5) or 10(6) TCID 50 of standard virus was markdely deppressed (Figure 1) by coinfection with supernatant from passage 3 of VRJ3 (VRJ1p1), VRJ1p1 supernatant also had interference activity as shown by coinfection with standard virus and expressed by plaque forming inhibition(Table 1). The plaque production of standard virus was inhibited by coinfection with VRJ1p1 supernatant which did not originate plaques when inoculated alone. The interference capacity of VRJ1p6 supernatant was reduced (Table 1) coincidentally with the formation of 55 PFU/ml. Interference activity was neutralized by Junin specific antiserum and inhibited by chloroform treatment. When Vero cells infected with VRJ1p6 supernatant were challenged with standard virus 72 hs later, an inhibition of 98% was achieved (Table 2) in contrast with value of 35% showed in Table 1.
Asunto(s)
Infecciones por Arbovirus , Células Cultivadas , Interferencia Viral , Animales , Arenavirus del Nuevo Mundo , Línea Celular , Haplorrinos , Técnicas In Vitro , Riñón , Dosificación Letal Mediana , Ratones , Factores de TiempoRESUMEN
Supernatants from Vero cells persistently infected with Junin virus interfered with cytolitic and lethal activities of standard virus. Two Vero cell sublines, chronically infected with Junin virus named VRJ1 and VRJ3, were obtained after prolonged cultivation of cells which survived primary infection. VFJ1 was maintained over a period of 48 days, by biweekly serial transfers while VRJ3, similarly treated, was cultivated for 385 days. One of the characteristics of these cell lines was resistance against superinfection with homologous virus that ordinaily produced CPE and plaques in normal Vero cells; the cells were then considered chronically infected. Supernatants taken at different cell passage level were tested for its interference activity after centrifugation to eliminate floating cells and debris. The degree of CPE intensity caused by inoculation of Vero cells with 10(4), 10(5) or 10(6) TCID 50 of standard virus was markdely deppressed (Figure 1) by coinfection with supernatant from passage 3 of VRJ3 (VRJ1p1), VRJ1p1 supernatant also had interference activity as shown by coinfection with standard virus and expressed by plaque forming inhibition(Table 1). The plaque production of standard virus was inhibited by coinfection with VRJ1p1 supernatant which did not originate plaques when inoculated alone. The interference capacity of VRJ1p6 supernatant was reduced (Table 1) coincidentally with the formation of 55 PFU/ml. Interference activity was neutralized by Junin specific antiserum and inhibited by chloroform treatment. When Vero cells infected with VRJ1p6 supernatant were challenged with standard virus 72 hs later, an inhibition of 98
was achieved (Table 2) in contrast with value of 35
showed in Table 1.
RESUMEN
Supernatants from Vero cells persistently infected with Junin virus interfered with cytolitic and lethal activities of standard virus. Two Vero cell sublines, chronically infected with Junin virus named VRJ1 and VRJ3, were obtained after prolonged cultivation of cells which survived primary infection. VFJ1 was maintained over a period of 48 days, by biweekly serial transfers while VRJ3, similarly treated, was cultivated for 385 days. One of the characteristics of these cell lines was resistance against superinfection with homologous virus that ordinaily produced CPE and plaques in normal Vero cells; the cells were then considered chronically infected. Supernatants taken at different cell passage level were tested for its interference activity after centrifugation to eliminate floating cells and debris. The degree of CPE intensity caused by inoculation of Vero cells with 10(4), 10(5) or 10(6) TCID 50 of standard virus was markdely deppressed (Figure 1) by coinfection with supernatant from passage 3 of VRJ3 (VRJ1p1), VRJ1p1 supernatant also had interference activity as shown by coinfection with standard virus and expressed by plaque forming inhibition(Table 1). The plaque production of standard virus was inhibited by coinfection with VRJ1p1 supernatant which did not originate plaques when inoculated alone. The interference capacity of VRJ1p6 supernatant was reduced (Table 1) coincidentally with the formation of 55 PFU/ml. Interference activity was neutralized by Junin specific antiserum and inhibited by chloroform treatment. When Vero cells infected with VRJ1p6 supernatant were challenged with standard virus 72 hs later, an inhibition of 98
was achieved (Table 2) in contrast with value of 35
showed in Table 1.