{"created":"2023-06-20T13:20:50.224282+00:00","id":894,"links":{},"metadata":{"_buckets":{"deposit":"af3b9bd1-b901-41a0-8624-5133c31c6025"},"_deposit":{"created_by":1,"id":"894","owners":[1],"pid":{"revision_id":0,"type":"depid","value":"894"},"status":"published"},"_oai":{"id":"oai:ir.soken.ac.jp:00000894","sets":["2:430:20"]},"author_link":["9854","9853","9852"],"item_1_creator_2":{"attribute_name":"著者名","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"安田, 二朗"}],"nameIdentifiers":[{"nameIdentifier":"9852","nameIdentifierScheme":"WEKO"}]}]},"item_1_creator_3":{"attribute_name":"フリガナ","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"ヤスダ, ジロウ"}],"nameIdentifiers":[{"nameIdentifier":"9853","nameIdentifierScheme":"WEKO"}]}]},"item_1_date_granted_11":{"attribute_name":"学位授与年月日","attribute_value_mlt":[{"subitem_dategranted":"1994-03-24"}]},"item_1_degree_grantor_5":{"attribute_name":"学位授与機関","attribute_value_mlt":[{"subitem_degreegrantor":[{"subitem_degreegrantor_name":"総合研究大学院大学"}]}]},"item_1_degree_name_6":{"attribute_name":"学位名","attribute_value_mlt":[{"subitem_degreename":"博士（理学）"}]},"item_1_description_12":{"attribute_name":"要旨","attribute_value_mlt":[{"subitem_description":"　　　Roles of viral NS and M proteins on the influenza virus growth were<br /> examined. The NS proteins of influenza virus, NS1I and NS2, are encoded<br /> by RNA segment 8. The NSI proitein is encoded by a colinear mRNA<br /> transcript, whereas thc NS2 protein with the molecular weight of 14.2<br /> kilodaltons (kDa) is synthesid after splicing of NSI mRNA. Up to now,<br /> these NS proteins are believed to exist only in virus-infected cells. The NSl<br /> protein, which localizes in nuclei of virus-infected cells, recognizes the <i>cis</i>-<br />acting sequence on NSI mRNA and controls its splicing to NS2 mRNA.<br /> NS2 is also present mainly in the nuclei. At present, however, little is<br /> known on the function of this protein. This study indicates that the NS2<br /> protein, previously considered as one of the two nonstructural proteins (NS 1<br /> and NS2), exists in virus particles as a structural component. By<br /> immunochemical method, the number of NS2 molecules in a virus particle<br /> was estimated to be 130-200 molecules. After solubilization of viral<br /> enve]ope, NS2 was still associated with ribonucleoprotein (RNP) cores, but<br /> was later dissociated from RNP upon removal of the membrane M1 protein.<br /> A filter-binding assay <i>in vitro</i> indlicated direct protein-protein contact<br /> between M1 ancl NS2. Following chemical cleavage of the M1 protein,<br /> NS2 was found to bincl only a C-terminal fragment of M1. By an<br /> immunoprecipitation method, NS2-M1 complexes were also detected in<br /> virus-infected cel] lysates. These observations altogether indicate specific<br /> molecu]ar nteraction between M1 and NS2, suggestlng that NS2 regulates<br /> the function of M1 or vice versa. <br />　　　The M gene of influenza viruses encodes 2 proteins, M1 and M2.<br /> The M 1 protein is tightly associated with virions forming a matrix, which<br /> associates with RNP at its internal surface but interacts with envelope at its<br /> external surface. M1 interacts with both NP, thereby interferes with the<br /> function of RNP-associated RNA polymerase, and NS2 in virions. In<br /> virus-infected cells, M1 is involved in both early (uncoating and import of<br /> RNP into infectecl nuc]ei) and late (assembly of virions during maturation<br /> and export of RNP from nuclei into cytoplasm) stages of virus growth. On<br /> the othcr hand, M2 forms an ion channel and is considered to control the<br /> transport of hemagglutinin (HA). M2 may also control uncoating step to<br /> release RNP in the early phase of virus infection. Genetic studies described<br /> in this report suggested that one or both of the M proteins have a regulatory<br /> role(s) of the rate of virus growth. Influenza virus A/WSN/33 forms large<br /> plaques (>3mm diameter) on MDCK cells whereas A/Aichi/2/68 forms<br /> on]y small plaques (<1mm diameter). Fast growing reassortants (AWM),<br /> isolated by mixed infection of MDCK cells with these two virus strains in<br /> the presence of anti-WSN antibodies, all carried the M gene from WSN.<br /> On MDCK cells, these reassortants produced progeny viruses as rapidly as<br /> did WSN, and the virus yield was as high as Aichi. Pulse-labeling<br /> experiments at various times after virus infectlon showed that the reassortant<br /> AWM started to synthesize viral proteins earlier than Aichi. To determine<br /> which of the two M proteins, M1 or M2, is responsible for the fast rate of<br /> virus growth, an attempt was made to make recombinant viruses possessing<br /> the chimeric M gene between WSN and Aichi. For this purpose, I<br /> employed a newly developed RNA-transfection method into helper virus-<br />infected cells. The ts-mutant derived from WSN, ts5 1 , carrying the ts lesion<br /> only in thc M gene, were used as a helper virus to rescue the chimeric M<br /> gene RNA. A transfectant virus carrying a chimeric M gene consisting of<br /> WSN-MI and Aichi-M2, CWA20, was generated by using an improved<br /> reverse genetics system. The CWA20 virus formed large-sized plaques,<br /> indicating that thc M1 protein, but not the M2 protein, was responsible for<br /> this rapid growth of WSN-type. Taken together, I conclude that the<br /> reassortant viruses entry into growth cycle faster than the parent Aichi strain,<br /> presumably due to rapid uncoating of the M1 protein from RNP cores. As a<br /> result of rapid uncoating, the reassortant RNP should be transported into<br /> host nuclei faster than Aichi RNP, ultimately leading to an early onset of<br /> transcription of the viral genes.","subitem_description_type":"Other"}]},"item_1_description_18":{"attribute_name":"フォーマット","attribute_value_mlt":[{"subitem_description":"application/pdf","subitem_description_type":"Other"}]},"item_1_description_7":{"attribute_name":"学位記番号","attribute_value_mlt":[{"subitem_description":"総研大甲第88号","subitem_description_type":"Other"}]},"item_1_select_14":{"attribute_name":"所蔵","attribute_value_mlt":[{"subitem_select_item":"有"}]},"item_1_select_8":{"attribute_name":"研究科","attribute_value_mlt":[{"subitem_select_item":"生命科学研究科"}]},"item_1_select_9":{"attribute_name":"専攻","attribute_value_mlt":[{"subitem_select_item":"18 遺伝学専攻"}]},"item_1_text_10":{"attribute_name":"学位授与年度","attribute_value_mlt":[{"subitem_text_value":"1993"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"YASUDA, Jiro","creatorNameLang":"en"}],"nameIdentifiers":[{"nameIdentifier":"9854","nameIdentifierScheme":"WEKO"}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2016-02-17"}],"displaytype":"simple","filename":"甲88_要旨.pdf","filesize":[{"value":"284.7 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"要旨・審査要旨 / Abstract, Screening Result","url":"https://ir.soken.ac.jp/record/894/files/甲88_要旨.pdf"},"version_id":"fb46043a-beea-4713-b2af-deeee2cd2f67"},{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2016-02-17"}],"displaytype":"simple","filename":"甲88_本文.pdf","filesize":[{"value":"1.8 MB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"本文","url":"https://ir.soken.ac.jp/record/894/files/甲88_本文.pdf"},"version_id":"ee0a8772-d403-42ed-9cc2-8152cfdec2b1"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"thesis","resourceuri":"http://purl.org/coar/resource_type/c_46ec"}]},"item_title":"インフルエンザウイルスの増殖の制御機構：ウイルス蛋白質の役割","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"インフルエンザウイルスの増殖の制御機構：ウイルス蛋白質の役割"},{"subitem_title":"Control of growth and assembly of influenza virus: Role of viral proteins","subitem_title_language":"en"}]},"item_type_id":"1","owner":"1","path":["20"],"pubdate":{"attribute_name":"公開日","attribute_value":"2010-02-22"},"publish_date":"2010-02-22","publish_status":"0","recid":"894","relation_version_is_last":true,"title":["インフルエンザウイルスの増殖の制御機構：ウイルス蛋白質の役割"],"weko_creator_id":"1","weko_shared_id":1},"updated":"2023-06-20T14:43:14.595559+00:00"}