Herpes Simplex Virus 1 γ 1 34.5 Protein Inhibits STING Activation That Restricts Viral Replication
Author:
Affiliation:
1. Department of Microbiology and Immunology, College of Medicine, University of Illinois, Chicago, Illinois, USA
2. Department of Biochemistry and Molecular Biology, College of Life Sciences, Nankai University, Tianjin, People's Republic of China
Abstract
Funder
National Natural Science Foundation of China
HHS | NIH | NIH Office of the Director
China Scholarship Council
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
Link
https://journals.asm.org/doi/pdf/10.1128/JVI.01015-18
Reference56 articles.
1. Herpes simplex virus infections
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3. Herpes simplex virus type 1 deletion variants 1714 and 1716 pinpoint neurovirulence-related sequences in Glasgow strain 17+ between immediate early gene 1 and the 'a' sequence
4. Replication, establishment of latency, and induced reactivation of herpes simplex virus gamma 1 34.5 deletion mutants in rodent models.
5. High-dose ocular infection with a herpes simplex virus type 1 ICP34.5 deletion mutant produces no corneal disease or neurovirulence yet results in wild-type levels of spontaneous reactivation
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