HIVは,エンドサイトーシスや,ダイナミン依存融合によるエンドソームとの融合を経由して細胞に侵入する
Kosuke Miyauchi1, Yuri Kim, Olga Latinovic
1Institute of Human Virology and Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Cell
|May 5, 2009
まとめ
ヒト免疫不全ウイルス (HIV-1) は,直接のプラズマ膜融合ではなく,エンドサイトーシス経由で細胞に侵入する. 完全な融合はエンドソーム内で起こり,ウイルスのグリコタンパク質とダイナミンに依存するプロセスです.
科学分野:
- ウイルス学 ウイルス学 ウイルス学
- 細胞生物学 細胞生物学
- 感染症 感染症は感染症です.
背景:
- 包装されたウイルスは,通常,pHに依存した内分泌体との融合経由で細胞に侵入する.
- HIV-1のようなpHに依存しないウイルスの侵入メカニズム,特に融合部位は未定義のままである.
- 以前の仮定では,HIV-1が宿主細胞のプラズマ膜と直接融合することを示唆していた.
研究 の 目的:
- HIV-1の侵入と融合の正確な場所とメカニズムを定義する.
- HIV-1感染におけるエンドサイトーシスと細胞内コンパートメントの役割を調査する.
- ダイナミンのような特定の細胞因子に対するHIV-1融合の依存度を決定する.
主な方法:
- 人口ベースのウイルスコンテンツのシトソールへの配送の測定.
- 単一のウイルス粒子の時間解像度イメージング.
- ダイナミン阻害剤であるダイナソールを用いた抑制研究.
主要な成果:
- 完全なHIV-1融合は,プラズマ膜ではなく,エンドソーム内で起こることが実証されました.
- プラズマ膜での融合は,脂質混合段階で停止した.
- HIV-1は,エンドソーム融合の前に受容体媒介の内細胞化を経験し,表皮質の露出を減少させます.
結論:
- HIV-1感染は,エンドサイトーシス経由で始まり,その後,細胞内エンドソーム内の融合が起こります.
- エンドソーム融合は,ウイルス包膜のグリコプロテインと宿主細胞のタンパク質ダイナミンに依存しています.
- このメカニズムは,HIV-1が侵入時に表面表皮質の曝露を最小限に抑えることで,免疫検出を回避するのを助けます.
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