Robust Virus-Specific Adaptive Immunity in COVID-19 Patients with SARS-CoV-2 Δ382 Variant Infection

J Clin Immunol. 2022 Feb;42(2):214-229. doi: 10.1007/s10875-021-01142-z. Epub 2021 Oct 30.

Abstract

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern (VOCs) that have become dominant as the pandemic progresses bear the ORF8 mutation together with multiple spike mutations. A 382-nucleotide deletion (Δ382) in the ORF7b and ORF8 regions has been associated with milder disease phenotype and less systemic inflammation in COVID-19 patients. However, its impact on host immunity against SARS-CoV-2 remains undefined. Here, RNA-sequencing was performed to elucidate whole blood transcriptomic profiles and identify contrasting immune signatures between patients infected with either wildtype or Δ382 SARS-CoV-2 variant. Interestingly, the immune landscape of Δ382 SARS-CoV-2 infected patients featured an increased adaptive immune response, evidenced by enrichment of genes related to T cell functionality, a more robust SARS-CoV-2-specific T cell immunity, as well as a more rapid antibody response. At the molecular level, eukaryotic initiation factor 2 signaling was found to be upregulated in patients bearing Δ382, and its associated genes were correlated with systemic levels of T cell-associated and pro-inflammatory cytokines. This study provides more in-depth insight into the host-pathogen interactions of ORF8 with great promise as a therapeutic target to combat SARS-CoV-2 infection.

Keywords: Adaptive immune response; Antibody response; CD4+ T cell response; CD8+ T cell response; COVID-19; ORF8; SARS-CoV-2; Transcriptome.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptive Immunity / immunology*
  • COVID-19 / immunology*
  • Cytokines / immunology
  • Host-Pathogen Interactions / immunology
  • Humans
  • Inflammation / immunology
  • Mutation / immunology
  • Pandemics / prevention & control
  • SARS-CoV-2 / immunology*
  • T-Lymphocytes / immunology

Substances

  • Cytokines

Supplementary concepts

  • SARS-CoV-2 variants