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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| Pubblicato in: | J Virol |
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| Autori principali: | , , |
| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
American Society for Microbiology (ASM)
1987
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| Soggetti: | |
| Accesso online: | 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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