ArticleVirulence2025
Immunodominant T cell responses to SARS-CoV-2 nucleocapsid protein in Omicron breakthrough infection post-inactivated vaccination.
Article in Virulence, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The Unexpected Visibility of the SARS-CoV-2 Nucleocapsid Protein Reveals a Hidden Route of Surface Trafficking.bioRxiv : the preprint server for biology · 2026Article
- Immunodominant T cell responses to SARS-CoV-2 nucleocapsid protein in Omicron breakthrough infection post-inactivated vaccination.Virulence · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The widespread administration of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines has not eliminated breakthrough infections due to immune evasion by viral mutations. Whether individuals with breakthrough infections can elicit effective T cell responses against the circulating Omicron JN.1 variant, and the specific immunodominant characteristics of these responses, remain to be elucidated. To address this, we recruited 93 individuals who had experienced early Omicron subvariant breakthrough infections following a three-dose regimen of inactivated SARS-CoV-2 vaccines. Intracellular cytokine staining was employed to evaluate T cell responses to the JN.1 nucleocapsid (N) protein overlapping peptide pool in peripheral blood mononuclear cells. Immunodominant epitopes were identified using a three-dimensional matrix screening approach. Human leukocyte antigen (HLA) blocking assays and truncated peptides stimulation assays were conducted to define the minimal epitope and HLA restriction. We found that breakthrough infections elicited robust CD4
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