Hsp90 Inhibitors Prevent HSV-1 Replication by Directly Targeting UL42-Hsp90 Complex

Hsp90 Inhibitors Prevent HSV-1 Replication by Directly Targeting UL42-Hsp90 Complex

Herpes simplex virus type I (HSV-1) is a member of the Alphaherpesvirinae family, which could initiate labial herpes caused by the reactivation of HSV-1 primary infection, and secondary infection even causes herpes encephalitis. The study presented here demonstrates that Hsp90 inhibitors (AT-533 and...

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Bibliographic Details
Published in:Frontiers in microbiology Vol. 12; p. 797279
Main Authors: Qin, Shurong, Hu, Xiao, Lin, Shimin, Xiao, Ji, Wang, Zhaoyang, Jia, Jiaoyan, Song, Xiaowei, Liu, Kaisheng, Ren, Zhe, Wang, Yifei
Format: Journal Article
Language:English
Published: Switzerland Frontiers Media S.A 03-02-2022
Subjects:
17-AAG
AT-533
DNA replication
HSV-1
Microbiology
protein docking
UL42
17-AAG
DNA replication
HSV-1
UL42
AT-533
protein docking
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Summary:Herpes simplex virus type I (HSV-1) is a member of the Alphaherpesvirinae family, which could initiate labial herpes caused by the reactivation of HSV-1 primary infection, and secondary infection even causes herpes encephalitis. The study presented here demonstrates that Hsp90 inhibitors (AT-533 and 17-AAG) directly targeted the HSV-1 UL42-Hsp90 complex, and Hsp90 interacted with HSV-1 UL42 in silicon and experiment. Interestingly, Hsp90 inhibitors also reduced virus titers of ACV-resistant clinical HSV-1 strains (153 and blue strain), revealing that HSV-1 UL42 would be a new target against ACV-resistant HSV-1 strains. Altogether, this present study indicates that Hsp90 inhibitors prevent HSV-1 proliferation by regulating the interaction between Hsp90 and HSV-1 UL42, suggesting a promising target for anti-HSV-1 therapies in the replication.
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Edited by: Chunfu Zheng, University of Calgary, Canada
This article was submitted to Virology, a section of the journal Frontiers in Microbiology
Reviewed by: Yi-Quan Wu, National Cancer Institute (NCI), United States; Bruce Z. Gao, Clemson University, United States
These authors have contributed equally to this work and share first authorship
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2021.797279