Serveur d'exploration H2N2

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Temperature-sensitive mutants of influenza virus

Identifieur interne : 002B68 ( Main/Exploration ); précédent : 002B67; suivant : 002B69

Temperature-sensitive mutants of influenza virus

Auteurs : Susan B. Spring [États-Unis] ; Sandra R. Nusinoff [États-Unis] ; John V. Mills [États-Unis] ; Douglas D. Richman [États-Unis] ; Eveline L. Tierney [États-Unis] ; Brian R. Murphy [États-Unis] ; Robert M. Chanock [États-Unis]

Source :

RBID : ISTEX:AC42964B887F98129724E3CC3DB76658E6D84F23

Descripteurs français

English descriptors

Abstract

Abstract: Temperature-sensitive genetic lesions were transferred from the ts-1 (H2N2) and ts-2 (H2N2) mutants of influenza A virus to wild-type influenza A (H3N2) virus by genetic reassortment. The ts-2 (H3N2) recombinants appeared to be homogeneous and did not undergo recombination with one another, suggesting that the original ts-2 mutant of influenza A (H2N2) contained a ts lesion(s) on only one RNA segment of its genome. In contrast the ts-1 (H3N2) recombinants fell into three phenotypic subsets which differed in degree of temperature sensitivity. Initially, the three subsets of ts-1 (H3N2) recombinants were thought to represent distinct complementation-recombination groups. However, complementation-recombination between the three subsets of ts-1 (H3N2) recombinants subsets was variable. Subsequent study indicated that mutants in each of the three subsets shared one ts lesion and two of the subsets shared an additional ts lesion. The mechanism whereby viruses of the three subsets which share one or two ts lesions, and nevertheless undergo apparent complementation-recombination on occasion is not understood.

Url:
DOI: 10.1016/0042-6822(75)90224-X


Affiliations:


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<front>
<div type="abstract" xml:lang="en">Abstract: Temperature-sensitive genetic lesions were transferred from the ts-1 (H2N2) and ts-2 (H2N2) mutants of influenza A virus to wild-type influenza A (H3N2) virus by genetic reassortment. The ts-2 (H3N2) recombinants appeared to be homogeneous and did not undergo recombination with one another, suggesting that the original ts-2 mutant of influenza A (H2N2) contained a ts lesion(s) on only one RNA segment of its genome. In contrast the ts-1 (H3N2) recombinants fell into three phenotypic subsets which differed in degree of temperature sensitivity. Initially, the three subsets of ts-1 (H3N2) recombinants were thought to represent distinct complementation-recombination groups. However, complementation-recombination between the three subsets of ts-1 (H3N2) recombinants subsets was variable. Subsequent study indicated that mutants in each of the three subsets shared one ts lesion and two of the subsets shared an additional ts lesion. The mechanism whereby viruses of the three subsets which share one or two ts lesions, and nevertheless undergo apparent complementation-recombination on occasion is not understood.</div>
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