Missense mutations in the VP1 gene of simian virus 40 that compensate for defects caused by deletions in the viral agnogene.

Simian virus 40 mutants lacking sequences in the late leader region are viable but produce smaller plaques than does wild-type virus. Within three passages at low multiplicities of infection, virus stocks of several such mutants accumulated variants that synthesized an altered form of the major viri...

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Detalles Bibliográficos

Publicado en:	J Virol
Principais autores:	Barkan, A, Welch, R C, Mertz, J E
Formato:	Artigo
Idioma:	Inglês
Publicado:	American Society for Microbiology (ASM) 1987
Assuntos:	Research Article
Acceso en liña:	https://ncbi.nlm.nih.govhttps://pmc.ncbi.nlm.nih.gov/articles/PMC255897/ https://ncbi.nlm.nih.govhttps://pubmed.ncbi.nlm.nih.gov/3041040/ https://ncbi.nlm.nih.govhttps://doi.org/10.1128/jvi.61.10.3190-3198.1987
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