| Project/Area Number |
06670326
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
ISHIMOTO Akinori Kyoto University, Institute. for Virus Research., Dep.of Viral Onc., Professor, ウイルス研究所, 教授 (50073127)
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| Co-Investigator(Kenkyū-buntansha) |
柳川 伸一 京都大学, ウイルス研究所, 助手 (70183978)
足立 昭夫 京都大学, ウイルス研究所, 助教授 (90127043)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Murine Leukemia Virus / Murine AIDS virus / マウス免疫不全症ウイルス |
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| Research Abstract |
The murine AIDS (MAIDS) virus has a unique sequence in its gag p12 region, which is responsible for MAIDS development. A transcript hybridizing with this sequence is expressed in normal C57BL/6 mice. This transcript has been proposed to be the origin of the MAIDS virus, since the virus was originally isolated from radiation-induced leukemic C57BL/6 mice. The transcript, designated Edv, has been previously cloned and sequenced (Kubo et al.1994. J.Gen.Virol.75 : 881-888). Compared with the nucleotide sequence of the helper LP-BM5 ecotropic virus, the pathogenic defective MAIDS virus has a total of 16-bp deletions and a 1-bp insertion in the 5' and 3' regions of the gag p12 sequence, respectively, and the Edv transcript contains only a 3-bp deletion. Therefore, the amino acid sequence of the defective MAIDS virus gag p12 region is not homologous to that of the helper virus and the Edv transcript due to the frameshift. These results demonstrated that the amino acid sequence homologous to the gag p12 region of the MAIDS virus resulting from the frameshift was essential for MAIDS development, and suggested that the MAIDS virus was generated by frameshift mutations in the gag p12 region of the Edv or a related sequence. On the other hand, the recovered sequences of the gag p12 region from the HGB-4M virus-infected mice had shared substitution mutations to proline, compared with the original HGB-4M sequence. The gag p12 region of the MAIDS virus is proline-rich. This suggested that the proline residues in the gag p12 region are impotant for MAIDS induction.
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