HSV-1-Driven Lipid Metabolic Reprogramming and Lipid Droplet Accumulation in Macrophages Impair Antiviral Immunity.

Authors

Junwen Ouyang, Yun He, Yaoyao Liu, Youmei Zheng, Changyu Wu, Jiaxuan Jiang, Kai Hu

Published in

Investigative ophthalmology & visual science. Volume 67. Issue 6. Pages 39. Jun 01, 2026.

Abstract

Herpes simplex virus type 1 (HSV-1) is a continuous health challenge, infecting 64% of the global population under the age of 50 years. Macrophages play a critical role in antiviral immunity by integrating metabolic status with effector functions. This study aimed to investigate how HSV-1 infection reshapes macrophage metabolism and to elucidate the consequent effects on innate and adaptive immune regulation.
We isolated bone marrow-derived macrophages (BMDMs) and assessed HSV-1-induced metabolic alterations using transcriptome sequencing, metabolomic profiling, and flow cytometry. We further used pharmacological inhibitors targeting key metabolic enzymes and co-culture system to evaluate macrophage functions. The main findings were validated in an in vivo mouse model of HSV-1 infection.
We found that HSV-1 infection induced marked lipid droplet (LD) accumulation in BMDMs. Pharmacological inhibition of diacylglycerol acyltransferase 2 (DGAT2) significantly reduced LD accumulation, limited viral replication, and enhanced the antiviral effector functions of macrophages.
Overall, our findings suggest that HSV-1-induced LD accumulation exerts a negative regulatory effect on macrophage immune function.

PMID:
42312920
Bibliographic data and abstract were imported from PubMed on 18 Jun 2026.

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