The mechanism of primate immunodeficiency viruses to broaden host range

2015 Fiscal Year Final Research Report

• Project/Area Number: 26860302
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Virology
• Research Institution: Tokyo Medical and Dental University (2015); Kyoto University (2014)
• Principal Investigator: Yoshida Takeshi 東京医科歯科大学, 医歯(薬)学総合研究科, 助教 (00727521)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: HIV-1 / レトロウイルス / 抗ウイルス蛋白質 / BST-2/tetherin / ウイルスの進化 / 霊長類 / エイズ / 種差

Outline of Final Research Achievements

Human immunodeficiency virus type 1 (HIV-1) is thought to have originated in Africa through the evolution of immunodeficiency viruses infecting wild chimpanzees (SIVcpz). Although animals including human beings possess intrinsic defense proteins called restriction factors, viruses had overcome them by evolution.
In this study, we found that an HIV-1 accessory protein Vpu binds to a human restriction factor BST-2 to degrade it and identified the important domain of Vpu to bind to BST-2. Since we found that Vpu of SIVcpz MB897, a close strain to the main group of HIV-1 in the phylogenetic tree, cannot bind to human BST-2, suggesting that Vpu of an ancient virus acquired an ability to bind to human BST-2 during the evolution.

Free Research Field

ウイルス学