Vero cells persistently infected with tacaribe virus: role of interfering particles in the establishment of the infection

Eight Vero cell sublines (Vero T) persistently infected with wild type Tacaribe virus replicated in different hosts were established. In order to unravel the mecha- nism involved in the initiation and maintenance of persistence, the properties of virus shed by the sublines and the presence of interf...

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Autor principal: D'Aiutolo, A.C
Otros Autores: Coto, C.E
Formato: Capítulo de libro
Lenguaje:Inglés
Publicado: 1986
Acceso en línea:Registro en Scopus
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Sumario:Eight Vero cell sublines (Vero T) persistently infected with wild type Tacaribe virus replicated in different hosts were established. In order to unravel the mecha- nism involved in the initiation and maintenance of persistence, the properties of virus shed by the sublines and the presence of interfering particles (IP) were analyzed. During the course of infection, persistent virus (Tac-pi) underwent muta- tions although no consistent pattern of virus evolution was observed, ts mutants were isolated from two Vero T sublines, whereas a slow growth variant was shed by another. The remaining sublines released virus resembling wt parental virus. Except for Vero T1 sublines, Vero T cultures shed no detectable IP. These results emphasize the point that neither the emergence of virus mutants nor the synthesis of IP is essential for the maintenance of the persistent state. To define the role of IP in the initiation of persistence, coinfection experiments with a characterized inoculum were performed. For that purpose, attempts were made to obtain IP stocks free from pfu by serial transfers of undiluted virus. Neither enrichment nor amplification of IP occurred, and virus stocks were freed of infectious virus by UV irradiation. If normal Vero cells were infected with Tac-pi virus released by Vero T2, Vero T3, Vero T4, Vero T5, Vero T6, Vero T7 and Vero T10 sublines, a complete destruction of the monolayer without cell recovery was ob- served. In contrast, parental and Vero T1 viruses always originated persistently infected sublines. Similarly, the addition of IP to virus inocula constituted by Tac-pi viruses released by Vero T2, Vero T3, Vero T4, Vero T5, Vero T6, Vero T7 and Vero T10 sublines gave rise to persistently infected cultures. These results suggest that although IP are not important by themselves in the maintenance of persistence, they play a major role in initiation. © 1986.
Bibliografía:Candurra, Damonte, Influence of cellular functions on the evolution of persistent infections with Junin virus (1985) Arch. Virol., 86, pp. 275-282
Coto, León, Peralta, Help, Laguens, Induction of infectious virus and viral surface antigens in Vero cells persistently infected with Junin virus (1979) Humoral Immunity and Neurological Diseases, pp. 405-415. , D. Karcher, A. Lowenthal, A.D. Strosberg, Plenum Press, New York
Damonte, Coto, Análisis de los factores que condicionan la formación de placas en células Vero infectadas con virus Junín y Tacaribe (1979) Revta. Asoc. Arg. Microbiol., 6, pp. 15-22
Damonte, Coto, Temperature sensitivity of the arenavirus Junin isolated from persistently infected Vero cells (1979) Intervirology, 11, pp. 282-287
Damonte, D'Aiutolo, Coto, Persistent infection of Tacaribe virus in Vero cells (1981) J. Gen. Virol., 65, pp. 41-48
Damonte, Mersich, Coto, Response of cells persistently infected with Arenaviruses to superinfection with homotypic and heterotypic viruses (1983) Virology, 129, pp. 474-478
Friedman, Ramseur, Mechanisms of persistent infections by cytopathic viruses in tissue culture (1979) Arch. Virol., 60, pp. 83-103
Gimenez, Compans, Defective interfering Tacaribe virus and persistently infected cells (1980) Virology, 107, pp. 229-239
Help, Coto, Propiedades de las partículas interferentes generadas por el virus Junín en células Vero (1981) Medicina (Bs. As.), 41, pp. 19-24
Holland, Levine, Mechanisms of virus persistence (1979) Cell, 14, pp. 447-452
Holland, Spindler, Horodyski, Graham, Nochol, Vandepol, Rapid evolution of RNA genomes (1982) Science, 215, pp. 1577-1585
Jacobson, Dutko, Pfau, Determinants of spontaneous recovery and persistence in MDCK cells infected with LCM virus (1979) J. Gen. Virol., 44, pp. 113-121
Oldstone, Holmstoen, Welsh, Jr., Alterations in acetylcholine enzyme in neuroblastoma cells persistently infected with LCM virus (1977) J. Cell. Physiol., 91, pp. 459-472
Preble, Youngner, ts viruses and etiology of chronic and inapparent infections (1975) J. Infect. Dis., 131, pp. 467-473
Rawls, Chan, Gee, Mechanisms of persistence in arenavirus infection: A brief report (1981) Can. J. Microbiol., 27, pp. 568-574
Ron, Tal, Coevolution of cells and virus as a mechanism of the persistence of Lymphotropic Minute virus of mice in L-cells (1985) J. Virol., 55, pp. 424-430
Sekellick, Marcus, Persistent infection. II. Interferon inducing temperature sensitive mutants as mediators of cells sparing: Possible role in persistent infection by vesicular stomatitis virus (1979) Virology, 95, pp. 36-47
Youngner, Preble, Evolution of viral populations (1980) Comprehensive Virology, 16, pp. 73-135. , H. Fraenkel-Conrat, R.R. Wagner, Plenum Press, New York
ISSN:01681702
DOI:10.1016/0168-1702(86)90072-9