STING facilitates nuclear import of herpesvirus genome during infection
Author(s) -
Yujin Hong,
Heena Jeong,
Kiwon Park,
Sungwon Lee,
Jae Youn Shim,
Hyewon Kim,
Yang Song,
Seowoo Park,
Hye Yoon Park,
V Narry Kim,
Kwangseog Ahn
Publication year - 2021
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.2108631118
Subject(s) - biology , nuclear transport , virology , capsid , herpes simplex virus , viral envelope , virus , sting , dna virus , viral entry , genome , gene , viral replication , microbiology and biotechnology , cell nucleus , genetics , engineering , aerospace engineering
Significance Human cytomegalovirus (HCMV) establishes lifelong latent infection in 60 to 90% of the population worldwide and constitutes a serious global health burden. For a successful infection, HCMV must overcome physical barriers: the plasma membrane and the nuclear envelope. Here, we report that the immune adaptor protein stimulator of interferon genes (STING), typically located in the endoplasmic reticulum, is a crucial host factor involved in the nuclear entry of HCMV. Without STING, the interaction between viral capsid and nuclear pore complex is defective, and HCMV fails to deliver the viral genome into the nucleus. In monocytes, STING deficiency prevents a successful establishment of HCMV persistence. This study offers a perspective for understanding HCMV uncoating and for developing interventions against herpesvirus infection.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom