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Published on: October 28, 2019
HSV-1 metabolic hijacking: Mechanisms to precision therapeutics
Siping Kuang1, Jingjing Zhang1, Junjie Chen1
1Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science and Technology, Xinjiang University, Urumqi, Xinjiang, China.
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Herpes Simplex Virus Type 1 (HSV-1) strategically reprograms host cell metabolism to fulfill its replicative needs and establish persistent infection. This hijacking extends across glucose, lipid, amino acid, and nucleotide pathways, diverting resources toward viral biosynthesis. Critically, the resulting metabolic landscape is not neutral but actively immunosuppressive. By altering the availability of key metabolites and cellular energy states, HSV-1 impairs the function of innate and adaptive immune cells, including antigen presentation by dendritic cells and the effector response of T cells, thereby enabling immune evasion. This review highlights that a systematic understanding of HSV-1-induced immunometabolic dysregulation reveals novel therapeutic targets. Exploiting these metabolic vulnerabilities - through pharmacological intervention or engineered oncolytic viruses - offers a promising precision medicine approach against HSV-1 infection and related pathologies.
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