Abstract
Herpes zoster results from latent varicella zoster virus reactivation in the dorsal root ganglia, causing blistering rash along the dermatomal distribution and post-herpetic neuralgia. Increasing studies indicated that there may be a correlation between herpes zoster and COVID-19. Nevertheless, the detailed pathophysiological mechanism is still unclear. We used bioinformatic analyses to study the potential genetic crosstalk between herpes zoster and COVID-19. COVID-19 and herpes zoster were associated with a similar subset of genes involved in “cytokine-cytokine receptor interaction,” “Jak-STAT signaling pathway,” and “IL-17 signaling pathway,” including TNF, IL10, ESR1, INFG, HLA-A, CRP, STAT3, IL6, IL7, and IL17A. Protein-protein interaction network assay showed that the combined gene set indicated a raised connectivity as compared to herpes zoster or COVID-19 alone, particularly the potentiated interactions with APOE, ARSA, CCR2, CCR5, CXCL13, EGFR, GAL, GP2, HLA-B, HLA-DRB1, IL5, TECTA, and THBS1, and these genes are related to “cytokine-cytokine receptor interaction”. Augmented Th17 cell differentiation and the resulting enhanced IL-17 signaling were identified in both COVID-19 and herpes zoster. Our data suggested aberrant interleukin-17 signaling as one possible mechanism through which COVID-19 could raise the risk of herpes zoster.
Keywords: Cytokine; Jak-STAT; SARS-CoV-2; Varicella zoster virus.
【저자키워드】 SARS-CoV-2, cytokine, Jak-STAT, Varicella zoster virus., 【초록키워드】 COVID-19, Genetic, Th17, IL6, risk, CRP, virus, receptor, EGFR, CXCL13, correlation, distribution, CCR5, Rash, mechanism, ApoE, TNF, HLA-B, Signaling, Interaction, STAT, Jak-STAT, IL-17, HLA-A, herpes zoster, interleukin-17, STAT3, CCR2, pathophysiological mechanism, IL17A, DRB1, ESR1, cytokine receptor, IL10, HLA-DRB1, cell differentiation, varicella, Varicella zoster virus, Zoster, ARSA, dorsal root ganglia, herpetic neuralgia, TECTA, THBS1, raise, resulting, involved, indicated, raised, suggested, analysis, subset, Increasing, IL5, blistering, GP2, Herpe, IL7, 【제목키워드】 mechanism, Signaling, Bioinformatic, analysis,