ArticleFrontiers in cellular and infection microbiology2026
Blood transcriptomic immune signatures in herpes zoster and postherpetic neuralgia: parallel cohort analyses of IFN-related pathway patterns.
Article in Frontiers in cellular and infection microbiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Herpes zoster (HZ) results from reactivation of latent varicella-zoster virus (VZV), and postherpetic neuralgia (PHN) is a major chronic pain complication. We performed parallel analyses of two independent public blood transcriptomic cohorts: GSE242252 (n=80; HZ onset, 1-year recovery, and controls) and PRJNA1142765 (n=23; 15 HZ and 8 PHN). Because the cohorts differed in platform, library preparation, design, and sampling structure, expression matrices were not merged; cross-cohort interpretation was restricted to within-cohort results and pathway-level directional concordance. HZ onset showed strong type I interferon (IFN)-dominated activation (HALLMARK_INTERFERON_ALPHA_RESPONSE, NES = 2.21, adjusted p=4.4x10-10), with recovery-associated attenuation of the sample-level IFN score (onset vs. recovery, p=0.005). In the smaller PHN cohort, only two genes met the strict differential-expression threshold, but Hallmark GSEA showed positive IFN-alpha and IFN-gamma enrichment. Ranking-sensitivity analysis confirmed IFN-alpha and IFN-gamma as the top two positively enriched Hallmark pathways using either log2 fold change or the DESeq2 Wald statistic, with leading-edge Jaccard similarities of 0.848 and 0.897, respectively. Exact patient-label permutation of the sample-level IFN score was not significant (two-sided p=0.297), although the PHN-minus-HZ direction remained positive in all 23 leave-one-out iterations. The new biological information is therefore an asymmetry of evidence: acute HZ IFN activation and recovery-associated attenuation are strongly supported, whereas the PHN-associated IFN pattern is stable at the pathway-ranking level but statistically uncertain at the patient level. Accordingly, the prior interpretation of persistent IFN activation in PHN is narrowed rather than reinforced. A structured external-replication search did not identify a suitable independent public human blood/PBMC transcriptomic cohort containing PHN samples; external evidence was therefore treated as literature-based concordance and supportive context rather than validation. Restricted computational prioritization highlighted IFN-related and CCL5/CCR5-associated axes for future study.
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