Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity

Herpes simplex virus type 1 (HSV-1) is a DNA virus that infects humans and establishes long-term latency within the host. Throughout its prolonged interaction with the host, HSV-1 evades the innate immune system by encoding its own proteins. Post-translational modifications (PTMs) of these proteins...

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Bibliographic Details
Main Authors: Yongxing Zhang, Junlei Xie, Ying Feng, Abdul Qadeer, Shanni Li, Xu Deng, Lipeng Zhu, Bo Kong, Zanxian Xia
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-02-01
Series:Frontiers in Microbiology
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Online Access:https://www.frontiersin.org/articles/10.3389/fmicb.2025.1543676/full
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Summary:Herpes simplex virus type 1 (HSV-1) is a DNA virus that infects humans and establishes long-term latency within the host. Throughout its prolonged interaction with the host, HSV-1 evades the innate immune system by encoding its own proteins. Post-translational modifications (PTMs) of these proteins play crucial roles in their function, activity, and interactions with other factors by modifying specific amino acids, thereby enabling a diverse range of protein functions. This review explores the mechanisms and roles of PTMs in HSV-1-encoded proteins, such as phosphorylation, ubiquitination, deamidation, and SUMOylation, during HSV-1 infection and latency. These modifications are essential for suppressing host innate immunity, facilitating viral replication, and elucidating the crosstalk among various post-translational modifications.
ISSN:1664-302X