The analysis of the mechanisms of HERV-K expression

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K21242
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Virology; Genetics/Chromosome dynamics
• Research Institution: Kumamoto University
• Principal Investigator: MONDE KAZUAKI 熊本大学, 大学院生命科学研究部(医), 助教 (70516137)
• Research Collaborator: Sawa Tomohiro 熊本大学, 大学院生命科学研究部, 教授 (30284756) ; MAEDA Yosuke 熊本大学, 大学院生命科学研究部, 准教授 (30284764) ; ONO Akira University of Michigan, Department of Microbiology and Immunology, Associate Professor ; Nagashima Kunio Leidos Biomedical Research, Inc, Frederick National Laboratory for Cancer Research・Electron Microscopy Laboratory, Professor
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: HERV-K / レトロトランスポゾン / 内在性レトロウイルス / HIV-1 / Gag / Sox2

Outline of Final Research Achievements

Human endogenous retroviruses (HERVs), the remnants of ancient retroviral infections, constitute about 8% of human genomic DNA. HERVs are costitutively transcribed in primordial germ cells. Eventually, HERV-K transcription is epigenetically silenced in somatic cells except for in pathological contexts. HERV-K expression is induced by HIV-1-infection in T cells. We found that HERV-K interferes the HIV-1 replication. HERV-K Gag MA, CA and NC are important for reduction of HIV-1 release and infectivity. It is conceivable that HERVs, which have adapted to human for a long time, might have protected the host from the threat of exogenous retroviruses. Our further analysis revealed that Sox2 is essential for the transcription of HERV-K. Interestingly, HERV-K had a retrotransposon activity and moved on the host genomes for a long-term culturing. It suggests that HERV-K is likely to be epigenetically regulated and play a role for development of embryo in short-term period of early development.

Free Research Field

ウイルス学