Assessment of immune #response induced by ChAdOx1 nCoV-19, Sputnik V, and BNT162b2 #vaccines during #COVID19 #outbreak in #Mexican population: Gene expression of the #cytokine storm

 

Highlights

    • The molecular immune response triggered by vaccines against COVID-19 was analyzed.

    • The evaluated genes were ACE2, CD79B, TMPRSS2, CTSB, FCGR3A and MB-1.

    • These vaccines induce a protective immune response through various mechanisms.

    • Vaccines regulate the immune response through pro- and anti-inflammatory cytokines.

Abstract

Introduction

COVID-19 vaccines using different technological platforms may induce distinct molecular responses. Characterizing gene-expression patterns after vaccination and in fatal COVID-19 may identify pathways associated with vaccination and severe disease.

Objective

To compare immune-, inflammatory-, and SARS-CoV-2-entry-related gene expression after AstraZeneca, Pfizer, or Sputnik V vaccination and with unvaccinated fatal COVID-19.

Materials and methods

Eighty Mexican adults were included: AstraZeneca (n = 19), Pfizer (n = 20), Sputnik (n = 21), and unvaccinated fatal COVID-19 (n = 20). Expression of 11 genes was measured by qPCR at days 30 (D30) and 60 (D60) after vaccination.

Statistical analysis

Longitudinal differences were analyzed by two-way repeated-measures ANOVA. Comparisons with fatal COVID-19 were exploratory. Benjamini–Hochberg correction controlled false discovery rate at 5%.

Results

No differences among vaccines were detected at D30. At D60, IL-10, IL-2, and CD79A differed among selected vaccine groups. Longitudinally, FCGR3A decreased in AstraZeneca and Sputnik, ACE2 decreased in Pfizer and Sputnik, and TMPRSS2 increased in Sputnik. Fatal COVID-19 showed predominantly higher expression of several genes than vaccinated groups. Notably, IL-2 and ACE2 were consistently higher in fatal COVID-19 than in all vaccinated groups at both time points.

Discussion and conclusions

Post-vaccination transcriptional profiles were dynamic, with selected differences emerging at D60, whereas fatal COVID-19 exhibited a distinct profile characterized predominantly by higher expression of immune-, inflammatory-, and viral-entry-related genes. Consistent IL-2 and ACE2 differences highlight molecular pathways potentially associated with severe disease. The observational design, however, precludes causal attribution to vaccination.

Perspectives

Longitudinal studies with appropriate controls are needed to establish the biological significance of these transcriptional patterns.

Source: 

Link: https://doi.org/10.1016/j.meegid.2026.106025

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