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

Yongxing Zhang; Junlei Xie; Ying Feng; Abdul Qadeer; Shanni Li; Xu Deng; Lipeng Zhu; Bo Kong; Zanxian Xia

doi:10.3389/fmicb.2025.1543676

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

Front Microbiol. 2025 Feb 11:16:1543676. doi: 10.3389/fmicb.2025.1543676. eCollection 2025.

Authors

Yongxing Zhang^#¹, Junlei Xie^#¹, Ying Feng¹, Abdul Qadeer¹, Shanni Li¹, Xu Deng², Lipeng Zhu³, Bo Kong⁴, Zanxian Xia^{1

5}

Affiliations

¹ Department of Cell Biology, School of Life Sciences, Central South University, Changsha, China.
² Xiangya School of Pharmaceutical Sciences, Central South University, Changsha, China.
³ School of Life Sciences, Xiangya School of Medicine, Central South University, Changsha, China.
⁴ China Tobacco Hunan Industrial, Changsha, China.
⁵ Hunan Key Laboratory of Animal Models for Human Diseases, Hunan Key Laboratory of Medical Genetics and Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, China.

^# Contributed equally.

Abstract

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.

Keywords: herpes simplex virus type 1; immune evasion; innate immunity; post-translational modifications; ubiquitination.

Publication types

Review

Grants and funding

The authors declare that financial support was received for the research, authorship, and/or publication of this article. This work was supported by the National Natural Science Foundation of China (82072293 and U21A20384), Science and Technology Innovation Plan of Hunan Province (2024WZ9001), Beijing Life Science Academy (BLSA, No: 2024100CB0170), the National Key Research and Development Program of China (2021YFC2300103), and the Natural Science Foundation of Hunan Province, China (2022JJ30692).