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characterizations and functions of influenza B virus BM2 protein.

乙型流感病毒BM2蛋白的特征和功能。

基本信息

批准号：
11670306
负责人：
ODAGIRI Takato
金额：
$ 1.92万
依托单位：
National Institute of Infectious Diseases (2000)Kanazawa Medical University (1999)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1999
资助国家：
日本
起止时间：
1999 至 2000
项目状态：
已结题

项目摘要

The influenza B virus genome RNA segment 7 encodes the M1 and the BM2 proteins. The BM2 protein is synthesized in a coupled translational termination-reinitiation mechanism at the overlapping stop-start penta-nucleotide in a bicistronic messenger RNA transcribed from RNA segment 7. However, features and functions of this protein remain unclear. We characterized the BM2 protein by using an antiserum raised to the BM2 protein of influenza B/Yamagata/1/73 strain. In cells infected with B/Yamagata virus the αBM2 antibody specifically detected the BM2 protein with M_r- 12 k and a polypeptide with M_r- 17 k. When infected cells were labeled with ^<32>Pi and immunoprecipitated with the αBM2 antibody, the ^<32>P-labeled 17 kD polypeptide was specifically precipitated. In the presence of casein kinase inhibitor, CKI-7, the synthesis of the 17 kD and the BM2 proteins was completely suppressed, although other viral proteins except for the polymerase protein were normally synthesized. These results suggested that the 17 kD species was a phosphorylated form of the BM2 protein. These species were substantially synthesized in the late phase of infection and localized in the cytoplasm throughout infection. Moreover, they were transported to the plasma membrane site and thereafter incorporated into virions. These results therefore suggest that the BM2 and the 17 kd proteins should be the components necessary for the life cycle of influenza B virus.

流感B病毒基因组RNA片段7编码M1和BM 2蛋白。BM 2蛋白在从RNA片段7转录的双顺反子信使RNA中重叠的终止-起始五核苷酸处以偶联的翻译终止-再起始机制合成。然而，这种蛋白的特征和功能仍不清楚。我们通过使用针对流感B/Yamagata/1/73株的BM 2蛋白的抗血清来表征BM 2蛋白。在感染B/Yamagata病毒的细胞中，α BM 2抗体特异性地检测到M_r- 12 k的BM 2蛋白和M_r- 17 k的多肽。当感染的细胞用^ Pi标记<32>并用α BM 2抗体免疫沉淀时，^<32>Pi标记的17 kD多肽被特异性沉淀。在酪蛋白激酶抑制剂CKI-7的存在下，17 kD和BM 2蛋白的合成被完全抑制，尽管除了聚合酶蛋白之外的其他病毒蛋白正常合成。这些结果表明，17 kD物质是BM 2蛋白的磷酸化形式。这些物质基本上是在感染后期合成的，并在整个感染过程中定位于细胞质中。此外，它们被运输到质膜位点，然后被并入病毒体。因此，这些结果表明，BM 2和17 kd蛋白应该是B型流感病毒生命周期所必需的组分。