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ORIGINAL RESEARCH article
Front. Microbiol.
Sec. Infectious Agents and Disease
Volume 16 - 2025 | doi: 10.3389/fmicb.2025.1560340
This article is part of the Research Topic Herpesvirus: Transmission, Pathogenesis, Host-Pathogen Interaction, Prevention and Treatment View all 4 articles
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The objective of this study was to investigate the effect of acyclovir (ACV) on the TLR9 signaling pathway after human immortalized epidermal (HaCaT) cell infection with herpes simplex virus type 2 (HSV-2).Methods: In this study, an in vitro cell model of HSV-2 infection was successfully constructed by infecting HaCaT with HSV-2 virus. In order to explore the antiviral mechanism of acyclovir (ACV), high-throughput transcriptome sequencing (RNA-seq) was used to analyze the genome-wide expression profiling of infected cells before and after ACV treatment, and to systematically compare the change characteristics of differentially expressed genes (DEGs). Based on the sequencing results, the study further focused on Toll-like receptor (TLR)9 signaling, using quantitative real-time reverse transcriptase chain reaction (qRT-PCR) to quantitatively detect the effect of ACV intervention on the mRNA expression level of key molecules of TLR 9 signaling pathway in HSV-2 infected HaCaT cells.Results: A total of 896 significant changes in gene expression were identified by the transcriptome analysis, including 314 upregulated genes and 582 downregulated genes. GO enrichment analysis showed that the differentially expressed genes were mainly related to CC includes the ubiquitin ligase complex 、 mitochondrial protein-containing complex 、 DNA-binding transcription activator activity 、 exonuclease activity、catabolic process、nuclear-transcribed mRNA catabolic process nuclear-transcribed mRNA catabolic process; KEGG enrichment analysis showed that the differentially expressed genes were mainly related to Toll-like receptor signaling pathway, herpes simplex virus 1 infection, and TNF signaling pathway.The RT-PCR results were confirmed to be basically consistent with the sequencing results.ACV altered the transcriptome level of HSV-2 infection in HaCaT cells.The RT-PCR results confirmed that ACV intervened in HSV-2 infection through the TLR9 signaling pathway.
Keywords: HSV - 2, Acyclovir, TLR9, RNA-Seq, HaCaT
Received: 14 Jan 2025; Accepted: 04 Mar 2025.
Copyright: © 2025 Shi, Kuang, Qi, Li and Wu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Lin Kuang, School of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, Changsha, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
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