Temperature-sensitive mutants of influenza virus: VI. Transfer of ts lesions from the Asian subtype of influenza a virus (H2N2) to the Hong Kong subtype (H3N2)
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, suggesti...
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| Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 1975-08, Vol.66 (2), p.522-532 |
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| container_title | Virology (New York, N.Y.) |
| container_volume | 66 |
| creator | Spring, Susan B Nusinoff, Sandra R Mills, John V Richman, Douglas D Tierney, Eveline L Murphy, Brian R Chanock, Robert M |
| description | 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. |
| doi_str_mv | 10.1016/0042-6822(75)90224-X |
| format | Article |
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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.</description><identifier>ISSN: 0042-6822</identifier><identifier>EISSN: 1096-0341</identifier><identifier>DOI: 10.1016/0042-6822(75)90224-X</identifier><identifier>PMID: 1171555</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Antigens, Viral - analysis ; Cattle ; Culture Techniques ; Fluorouracil ; Genetic Complementation Test ; Humans ; Influenza A virus - growth & development ; Influenza A virus - immunology ; Influenza A virus - radiation effects ; Influenza A Virus, H2N2 Subtype ; Influenza A Virus, H3N2 Subtype ; Kidney ; Macaca mulatta ; Mutagens ; Mutation ; Orthomyxoviridae - growth & development ; Radiation Effects ; Recombination, Genetic ; Temperature ; Ultraviolet Rays ; Viral Plaque Assay</subject><ispartof>Virology (New York, N.Y.), 1975-08, Vol.66 (2), p.522-532</ispartof><rights>1975</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/004268227590224X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/1171555$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Spring, Susan B</creatorcontrib><creatorcontrib>Nusinoff, Sandra R</creatorcontrib><creatorcontrib>Mills, John V</creatorcontrib><creatorcontrib>Richman, Douglas D</creatorcontrib><creatorcontrib>Tierney, Eveline L</creatorcontrib><creatorcontrib>Murphy, Brian R</creatorcontrib><creatorcontrib>Chanock, Robert M</creatorcontrib><title>Temperature-sensitive mutants of influenza virus: VI. Transfer of ts lesions from the Asian subtype of influenza a virus (H2N2) to the Hong Kong subtype (H3N2)</title><title>Virology (New York, N.Y.)</title><addtitle>Virology</addtitle><description>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.</description><subject>Animals</subject><subject>Antigens, Viral - analysis</subject><subject>Cattle</subject><subject>Culture Techniques</subject><subject>Fluorouracil</subject><subject>Genetic Complementation Test</subject><subject>Humans</subject><subject>Influenza A virus - growth & development</subject><subject>Influenza A virus - immunology</subject><subject>Influenza A virus - radiation effects</subject><subject>Influenza A Virus, H2N2 Subtype</subject><subject>Influenza A Virus, H3N2 Subtype</subject><subject>Kidney</subject><subject>Macaca mulatta</subject><subject>Mutagens</subject><subject>Mutation</subject><subject>Orthomyxoviridae - growth & development</subject><subject>Radiation Effects</subject><subject>Recombination, Genetic</subject><subject>Temperature</subject><subject>Ultraviolet Rays</subject><subject>Viral Plaque Assay</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1975</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVUV1LwzAUDaLo_PgHCnmcD51J2iSrD8IQteLQlym-hbS91cialiQdzD_jX7V1U_DlXi7ng8s5CJ1SMqGEigtCEhaJKWNjyc9TwlgSve6gESWpiEic0F00-qMcoEPvP0h_S0n20T6lknLOR-hrAXULTofOQeTBehPMCnDdBW2Dx02Fja2WHdhPjVfGdf4Sv9xP8MJp6ytwA6GnLcGbxnpcuabG4R3wzBttse_ysG7hv8vWB48z9sjOcWh-BFlj3_DDMH5F4yzu8WO0V-mlh5PtPkLPtzeL6yyaP93dX8_mEVApQkSThIhUEMHSoqCMUw2acYiLqSYynZKKV4VkTEjBBC0hJTmkvOR5DCSf0oLHR-hs49t2eQ2lap2ptVurbVA9frXBoX9iZcApXxiwBZTGQRFU2RhFiRqKUUPqakhdSa5-ilGv8TdW-38j</recordid><startdate>197508</startdate><enddate>197508</enddate><creator>Spring, Susan B</creator><creator>Nusinoff, Sandra R</creator><creator>Mills, John V</creator><creator>Richman, Douglas D</creator><creator>Tierney, Eveline L</creator><creator>Murphy, Brian R</creator><creator>Chanock, Robert M</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>197508</creationdate><title>Temperature-sensitive mutants of influenza virus: VI. Transfer of ts lesions from the Asian subtype of influenza a virus (H2N2) to the Hong Kong subtype (H3N2)</title><author>Spring, Susan B ; Nusinoff, Sandra R ; Mills, John V ; Richman, Douglas D ; Tierney, Eveline L ; Murphy, Brian R ; Chanock, Robert M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e176t-14406960629cc1251aea25e3c8a07980f5fc722676261de90be95d5b3e0b81c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1975</creationdate><topic>Animals</topic><topic>Antigens, Viral - analysis</topic><topic>Cattle</topic><topic>Culture Techniques</topic><topic>Fluorouracil</topic><topic>Genetic Complementation Test</topic><topic>Humans</topic><topic>Influenza A virus - growth & development</topic><topic>Influenza A virus - immunology</topic><topic>Influenza A virus - radiation effects</topic><topic>Influenza A Virus, H2N2 Subtype</topic><topic>Influenza A Virus, H3N2 Subtype</topic><topic>Kidney</topic><topic>Macaca mulatta</topic><topic>Mutagens</topic><topic>Mutation</topic><topic>Orthomyxoviridae - growth & development</topic><topic>Radiation Effects</topic><topic>Recombination, Genetic</topic><topic>Temperature</topic><topic>Ultraviolet Rays</topic><topic>Viral Plaque Assay</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Spring, Susan B</creatorcontrib><creatorcontrib>Nusinoff, Sandra R</creatorcontrib><creatorcontrib>Mills, John V</creatorcontrib><creatorcontrib>Richman, Douglas D</creatorcontrib><creatorcontrib>Tierney, Eveline L</creatorcontrib><creatorcontrib>Murphy, Brian R</creatorcontrib><creatorcontrib>Chanock, Robert M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Virology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Spring, Susan B</au><au>Nusinoff, Sandra R</au><au>Mills, John V</au><au>Richman, Douglas D</au><au>Tierney, Eveline L</au><au>Murphy, Brian R</au><au>Chanock, Robert M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Temperature-sensitive mutants of influenza virus: VI. Transfer of ts lesions from the Asian subtype of influenza a virus (H2N2) to the Hong Kong subtype (H3N2)</atitle><jtitle>Virology (New York, N.Y.)</jtitle><addtitle>Virology</addtitle><date>1975-08</date><risdate>1975</risdate><volume>66</volume><issue>2</issue><spage>522</spage><epage>532</epage><pages>522-532</pages><issn>0042-6822</issn><eissn>1096-0341</eissn><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.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>1171555</pmid><doi>10.1016/0042-6822(75)90224-X</doi><tpages>11</tpages></addata></record> |
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| ispartof | Virology (New York, N.Y.), 1975-08, Vol.66 (2), p.522-532 |
| issn | 0042-6822 1096-0341 |
| language | eng |
| recordid | cdi_pubmed_primary_1171555 |
| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Antigens, Viral - analysis Cattle Culture Techniques Fluorouracil Genetic Complementation Test Humans Influenza A virus - growth & development Influenza A virus - immunology Influenza A virus - radiation effects Influenza A Virus, H2N2 Subtype Influenza A Virus, H3N2 Subtype Kidney Macaca mulatta Mutagens Mutation Orthomyxoviridae - growth & development Radiation Effects Recombination, Genetic Temperature Ultraviolet Rays Viral Plaque Assay |
| title | Temperature-sensitive mutants of influenza virus: VI. Transfer of ts lesions from the Asian subtype of influenza a virus (H2N2) to the Hong Kong subtype (H3N2) |
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