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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Frontiers Media S.A.
2025-02-01
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| 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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| author | Yongxing Zhang Junlei Xie Ying Feng Abdul Qadeer Shanni Li Xu Deng Lipeng Zhu Bo Kong Zanxian Xia Zanxian Xia |
| author_facet | Yongxing Zhang Junlei Xie Ying Feng Abdul Qadeer Shanni Li Xu Deng Lipeng Zhu Bo Kong Zanxian Xia Zanxian Xia |
| author_sort | Yongxing Zhang |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-954c589d1bbd4d8abf2f008877c7c93e |
| institution | Kabale University |
| issn | 1664-302X |
| language | English |
| publishDate | 2025-02-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Microbiology |
| spelling | doaj-art-954c589d1bbd4d8abf2f008877c7c93e2025-02-11T06:59:04ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2025-02-011610.3389/fmicb.2025.15436761543676Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunityYongxing Zhang0Junlei Xie1Ying Feng2Abdul Qadeer3Shanni Li4Xu Deng5Lipeng Zhu6Bo Kong7Zanxian Xia8Zanxian Xia9Department of Cell Biology, School of Life Sciences, Central South University, Changsha, ChinaDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha, ChinaDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha, ChinaDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha, ChinaDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha, ChinaXiangya School of Pharmaceutical Sciences, Central South University, Changsha, ChinaSchool of Life Sciences, Xiangya School of Medicine, Central South University, Changsha, ChinaChina Tobacco Hunan Industrial, Changsha, ChinaDepartment of Cell Biology, School of Life Sciences, Central South University, Changsha, ChinaHunan 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, ChinaHerpes 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.https://www.frontiersin.org/articles/10.3389/fmicb.2025.1543676/fullherpes simplex virus type 1innate immunityimmune evasionpost-translational modificationsubiquitination |
| spellingShingle | Yongxing Zhang Junlei Xie Ying Feng Abdul Qadeer Shanni Li Xu Deng Lipeng Zhu Bo Kong Zanxian Xia Zanxian Xia Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity Frontiers in Microbiology herpes simplex virus type 1 innate immunity immune evasion post-translational modifications ubiquitination |
| title | Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity |
| title_full | Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity |
| title_fullStr | Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity |
| title_full_unstemmed | Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity |
| title_short | Post-translational modifications as a key mechanism for herpes simplex virus type I evasion of host innate immunity |
| title_sort | post translational modifications as a key mechanism for herpes simplex virus type i evasion of host innate immunity |
| topic | herpes simplex virus type 1 innate immunity immune evasion post-translational modifications ubiquitination |
| url | https://www.frontiersin.org/articles/10.3389/fmicb.2025.1543676/full |
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