Investigation of the molecular mechanism of AIDS virus evolution

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K07166
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Evolutionary biology
• Research Institution: Kyoto University
• Principal Investigator: Sato Kei 京都大学, ウイルス・再生医科学研究所, 講師 (10593684)
• Co-Investigator(Renkei-kenkyūsha): Koyanagi Yoshio 京都大学・ウイルス, 再生医科学研究所, 教授 (80215417) ; Iwasa You 九州大学, 理学研究院, 教授 (70176535) ; Iwami Shingo 九州大学, 理学研究院, 准教授 (90518119) ; Ren FengRong 東京医科歯科大学, 難治疾患研究所, 特任准教授 (60280989) ; Nakagawa So 東海大学, 医学部, 講師 (70510014)
• Research Collaborator: Dong Sung An カリフォルニア大学ロサンゼルス校, 教授
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: システムウイルス学 / HIV-1 / チンパンジー / ヒト化マウス / 適応進化

Outline of Final Research Achievements

HIV-1, the causative agent of AIDS, is originated from SIVcpz, the chimpanzee precursor of the human virus, approximately 100 years ago. This indicates that HIV-1 has emerged through the cross-species transmission of SIVcpz from chimpanzees to humans. However, it remains unclear how SIVcpz has evolved into pandemic HIV-1 in humans. To address this question, we used three SIVcpz (MB897, EK505, and MT145), four pandemic HIV-1 (NL4-3, NLCSFV3, JRCSF and AD8) and 2 non-pandemic HIV-1 (YBF30 and DJO0131) strains and humanized mouse model. This is the first experimental investigation to use an animal model to demonstrate a gain-of-function evolution of SIVcpz into pandemic HIV-1.

Free Research Field

ウイルス学