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Construction of a pathological model of skin lesions in acute herpes zoster virus infection and its molecular mechanism

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Abstract

Varicella-zoster virus (VZV), a common pathogen with humans as the sole host, causes primary infection and undergoes a latent period in sensory ganglia. The recurrence of VZV is often accompanied by severe neuralgia in skin tissue, which has a serious impact on the life of patients. During the acute infection of VZV, there are few related studies on the pathophysiological mechanism of skin tissue. In this study, transcriptome sequencing data from the acute response period within 2 days of VZV antigen stimulation of the skin were used to explore a model of the trajectory of skin tissue changes during VZV infection. It was found that early VZV antigen stimulation caused activation of mainly natural immune-related signaling pathways, while in the late phase activation of mainly active immune-related signaling pathways. JAK-STAT, NFκB, and TNFα signaling pathways are gradually activated with the progression of infection, while Hypoxia is progressively inhibited. In addition, we found that dendritic cell-mediated immune responses play a dominant role in the lesion damage caused by VZV antigen stimulation of the skin. This study provides a theoretical basis for the study of the molecular mechanisms of skin lesions during acute VZV infection.

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Data availability

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

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Concept: [Hao Zhou] and [Zheng Ye]; Design: [Hao Zhou], [Yanjun Sun] and [Bo Sun]; Supervision: [Bo Sun]; Resources: [Bo Sun]; Materials: [Hao Zhou] and [Zheng Ye]; Data Collection and/or Processing: [Hao Zhou] and [Zheng Ye]; Analysis and/or Interpretation: [Hao Zhou] and [Zheng Ye]; Literature Search: [Hao Zhou], [Zheng Ye], [Zhao Gao], [Chengxi Xi] and [Jinxia Yin]; Writing Manuscript: [Hao Zhou] and [Zheng Ye]; Critical Review: [Bo Sun].

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Correspondence to Yanjun Sun or Bo Sun.

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Zhou, H., Ye, Z., Gao, Z. et al. Construction of a pathological model of skin lesions in acute herpes zoster virus infection and its molecular mechanism. Mamm Genome (2024). https://doi.org/10.1007/s00335-024-10039-2

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