Coevolution of cells and viruses in a persistent infection of foot-and-mouth disease virus in cell culture
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| Published in | Journal of Virology Vol. 62; no. 6; pp. 2050 - 2058 |
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| Main Authors | , , , , , , , |
| Format | Journal Article |
| Language | English |
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Washington, DC
American Society for Microbiology
01.06.1988
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| ISSN | 0022-538X 1098-5514 |
| DOI | 10.1128/jvi.62.6.2050-2058.1988 |
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Virus and cells evolve during serial passage of cloned BHK-21 cells persistently infected with foot-and-mouth disease virus (FMDV). These carrier cells, termed C1-BHK-Rc1 (J.C. de la Torre, M. Dávila, F. Sobrino, J. Ortín, and E. Domingo, Virology 145:24-35, 1985), become constitutively resistant to the parental FMDV C-S8c1. Curing of late-passage C1-BHK-Rc1 cells of FMDV by ribavirin treatment (J.C. de la Torre, B. Alarcón, E. Martínez-Salas, L. Carrasco, and E. Domingo, J. Virol. 61:233-235, 1987) did not restore sensitivity to FMDV C-S8c1. The resistance of C1-BHK-Rc1 cells to FMDV C-S8c1 was not due to an impairment of attachment, penetration, or uncoating of the particles but to some intracellular block that resulted in a 100-fold decrease in the amount of FMDV RNA in the infected cells. FMDV R59, the virus isolated from late-passage carrier cells, partly overcame the cellular block and was more cytolytic than FMDV C-S8c1 for BHK-21 cells. Sequencing of the VP1 gene from nine viral clones from C1-BHK-Rc1 cells showed genetic heterogeneity of 5 X 10(-4) substitutions per nucleotide. Mutations were sequentially fixed during persistence. In addition to resistance to FMDV C-S8c1, C1-BHK-Rc1 cells showed a characteristic round cell morphology, and compared with BHK-21 cells, they grew faster in liquid culture, were less subject to contact inhibition of growth, and had an increased ability to form colonies in semisolid agar. Reconstitution of a persistent infection was readily attained with late-passage C1-BHK-Rc1 cells and FMDV C-S8c1 or FMDV R59. The results suggest that coevolution of BHK-21 cells and FMDV contributes to the maintenance of persistence in cell culture.Virus and cells evolve during serial passage of cloned BHK-21 cells persistently infected with foot-and-mouth disease virus (FMDV). These carrier cells, termed C1-BHK-Rc1 (J.C. de la Torre, M. Dávila, F. Sobrino, J. Ortín, and E. Domingo, Virology 145:24-35, 1985), become constitutively resistant to the parental FMDV C-S8c1. Curing of late-passage C1-BHK-Rc1 cells of FMDV by ribavirin treatment (J.C. de la Torre, B. Alarcón, E. Martínez-Salas, L. Carrasco, and E. Domingo, J. Virol. 61:233-235, 1987) did not restore sensitivity to FMDV C-S8c1. The resistance of C1-BHK-Rc1 cells to FMDV C-S8c1 was not due to an impairment of attachment, penetration, or uncoating of the particles but to some intracellular block that resulted in a 100-fold decrease in the amount of FMDV RNA in the infected cells. FMDV R59, the virus isolated from late-passage carrier cells, partly overcame the cellular block and was more cytolytic than FMDV C-S8c1 for BHK-21 cells. Sequencing of the VP1 gene from nine viral clones from C1-BHK-Rc1 cells showed genetic heterogeneity of 5 X 10(-4) substitutions per nucleotide. Mutations were sequentially fixed during persistence. In addition to resistance to FMDV C-S8c1, C1-BHK-Rc1 cells showed a characteristic round cell morphology, and compared with BHK-21 cells, they grew faster in liquid culture, were less subject to contact inhibition of growth, and had an increased ability to form colonies in semisolid agar. Reconstitution of a persistent infection was readily attained with late-passage C1-BHK-Rc1 cells and FMDV C-S8c1 or FMDV R59. The results suggest that coevolution of BHK-21 cells and FMDV contributes to the maintenance of persistence in cell culture. Virus and cells evolve during serial passage of cloned BHK-21 cells persistently infected with foot-and-mouth disease virus (FMDV). These carrier cells, termed C1-BHK-Rc1 (J.C. de la Torre, M. Dávila, F. Sobrino, J. Ortín, and E. Domingo, Virology 145:24-35, 1985), become constitutively resistant to the parental FMDV C-S8c1. Curing of late-passage C1-BHK-Rc1 cells of FMDV by ribavirin treatment (J.C. de la Torre, B. Alarcón, E. Martínez-Salas, L. Carrasco, and E. Domingo, J. Virol. 61:233-235, 1987) did not restore sensitivity to FMDV C-S8c1. The resistance of C1-BHK-Rc1 cells to FMDV C-S8c1 was not due to an impairment of attachment, penetration, or uncoating of the particles but to some intracellular block that resulted in a 100-fold decrease in the amount of FMDV RNA in the infected cells. FMDV R59, the virus isolated from late-passage carrier cells, partly overcame the cellular block and was more cytolytic than FMDV C-S8c1 for BHK-21 cells. Sequencing of the VP1 gene from nine viral clones from C1-BHK-Rc1 cells showed genetic heterogeneity of 5 X 10(-4) substitutions per nucleotide. Mutations were sequentially fixed during persistence. In addition to resistance to FMDV C-S8c1, C1-BHK-Rc1 cells showed a characteristic round cell morphology, and compared with BHK-21 cells, they grew faster in liquid culture, were less subject to contact inhibition of growth, and had an increased ability to form colonies in semisolid agar. Reconstitution of a persistent infection was readily attained with late-passage C1-BHK-Rc1 cells and FMDV C-S8c1 or FMDV R59. The results suggest that coevolution of BHK-21 cells and FMDV contributes to the maintenance of persistence in cell culture. Virus and cells evolve during serial passage of cloned BHK-21 cells persistently infected with foot-and-mouth disease virus (FMDV). These carrier cells, termed C sub(1)-BHK-Rc1, become constitutively resistant to the parental FMDV C-S8c1. Curing of late-passage C sub(1)-BHK-Rc1 cells of FMDV by ribavirin treatment did not restore sensitivity to FMDV C-S8c1. The resistance of C sub(1)-BHK-Rc1 cells to FMDV C-S8c1 was not due to an impairment of attachment, penetration, or uncoating of the particles but to some intracellular block that resulted in a 100-fold decrease in the amount of FMDV RNA in the infected cells. FMDV R59, the virus isolated from late-passage carrier cells, partly overcame the cellular block and was more cytolytic than FMDV C-S8c1 for BHK-21 cells. Sequencing of the VP1 gene from nine viral clones from C sub(1)-BHK-Rc1 cells showed genetic heterogeneity of 5 x 10 super(-4) substitutions per nucleotide. |
| Author | Domingo, E Torre, J.C. de la Martinez-Salas, E Gebauer, F Diez, J Rocha, E Villaverde, A Davila, M |
| AuthorAffiliation | Centro de Biología Molecular (Consejo Superior de Investigaciones Científicas), Universidad Autónoma de Madrid, Spain |
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| Keywords | Virus Aphthovirus Cell culture Molecular evolution RNA Picornaviridae Biological evolution Persistent infection Morphology Aphthovirus C Infected cell Host virus relation |
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Mendeley... Virus and cells evolve during serial passage of cloned BHK-21 cells persistently infected with foot-and-mouth disease virus (FMDV). These carrier cells, termed... |
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| StartPage | 2050 |
| SubjectTerms | Animals APHTHOVIRUS Aphthovirus - genetics Aphthovirus - growth & development Base Sequence Biological and medical sciences biosynthesis BOVIN CATTLE CELL CULTURE Cell Division Cell Line Cells, Cultured Cells, Cultured - cytology Cells, Cultured - microbiology CERDO Cricetinae CULTIVO DE CELULAS CULTURE DE CELLULES cytology Endocytosis EVOLUCION EVOLUTION foot-and-mouth disease virus Fundamental and applied biological sciences. Psychology GANADO BOVINO genetics growth & development INFECCIONES INFECTION Microbiology Molecular Sequence Data Mutation PORCIN Replicative cycle, interference, host-virus relations, pathogenicity, miscellaneous strains RNA, Viral RNA, Viral - biosynthesis SWINE Time Factors Transfection Virology VIRUS FIEBRE AFTOSA VIRUS FIEVRE APHTEUSE Virus Replication |
| Title | Coevolution of cells and viruses in a persistent infection of foot-and-mouth disease virus in cell culture |
| URI | http://jvi.asm.org/content/62/6/2050.abstract https://www.ncbi.nlm.nih.gov/pubmed/2835509 https://www.proquest.com/docview/15036581 https://www.proquest.com/docview/49779445 https://www.proquest.com/docview/78220062 https://pubmed.ncbi.nlm.nih.gov/PMC253290 |
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