Bioinformatic analyses suggest augmented interleukin-17 signaling as the mechanism of COVID-19-associated herpes zoster.
Environ Sci Pollut Res Int
; 28(46): 65769-65775, 2021 Dec.
Article
in English
| MEDLINE | ID: covidwho-1330399
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
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Signal Transduction
/
Interleukin-17
/
COVID-19
/
Herpes Zoster
Type of study:
Prognostic study
Topics:
Long Covid
Limits:
Humans
Language:
English
Journal:
Environ Sci Pollut Res Int
Journal subject:
Environmental Health
/
Toxicology
Year:
2021
Document Type:
Article
Affiliation country:
S11356-021-15567-x
Similar
MEDLINE
...
LILACS
LIS