HLA-B*15:01-positive severe COVID-19 patients lack CD8+ T cell pools with highly expanded public clonotypes

Louise C Rowntree, Lilith F Allen, Ruth R Hagen, Hayley A McQuilten, Ahmed A Quadeer, Priyanka Chaurasia, Prathanporn Kaewpreedee, Kelly W K Lee, Carolyn A Cohen, Jan Petersen, Dene R Littler, Jennifer R Habel, Wuji Zhang, Samuel M S Cheng, Ken Ka Pang Chan, Janette S Y Kwok, Kathy S M Leung, Joseph T Wu, Cheuk-Kwong Lee, Jane DaviesPia S Pannaraj, E Kaity Allen, Paul G Thomas, Shidan Tosif, Nigel W Crawford, Martha Lappas, Irani Thevarajan, Sharon R Lewin, Stephen J Kent, Jennifer A Juno, Katherine A Bond, Deborah A Williamson, Natasha E Holmes, Olivia C Smibert, Claire L Gordon, Jason A Trubiano, Tom C Kotsimbos, Allen C Cheng, Claudia Efstathiou, Lance Turtle, Ryan S Thwaites, Christopher E Brightling, PHOSP-COVID Collaborative Group, Jamie Rossjohn, Matthew R McKay, Jinmin Tian, William Jun Liu, George Fu Gao, Jianqing Xu, Kyuto Sonehara, Ken J Ishii, Ho Namkoong, Yukinori Okada, Malik Peiris, David S. C. Hui, Leo L. M. Poon, Peter C. Doherty*, Thi H. O. Nguyen*, Sophie A. Valkenberg*, Katherine Kedzierska*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Understanding host factors driving asymptomatic versus severe disease outcomes is of key importance if we are to control emerging and re-emerging viral infections. HLA-B*15:01 has been associated with asymptomatic SARS-CoV-2 infection in nonhospitalized individuals of European ancestry, with protective immunity attributed to preexisting cross-reactive CD8+ T-cells directed against HLA-B*15:01-restricted Spike-derived S919-927 peptide (B15/S919+CD8+ T-cells). However, fundamental questions remained on the abundance and clonotypic nature of CD8+ T-cell responses in HLA-B*15:01-positive patients who succumbed to life-threatening COVID-19. Here, we analyzed B15/S919+CD8+ T-cell responses in COVID-19 patients from independent HLA-typed COVID-19 patient cohorts across three continents, Australia, Asia and Europe. We assessed B15/S919+CD8+ T-cells in COVID-19 patients across disease outcomes ranging from asymptomatic to hospitalized critical illness. We found that severe/critical COVID-19 patients mounted B15/S919+CD8+ T-cell responses lacking a highly expanded key public B15/S919+CD8+ T-cell receptor (TCR; TRAV9-2/TRBV7-2) which recurred across multiple individuals in COVID-19 patients with a mild disease. Instead, B15/S919+CD8+ T-cell responses in life-threatening disease had a prevalence of an alternate TCR clonotypic motif (TRAV38-2/DV8/TRBV20-1), potentially contributing, at least in part, to why B15/S919+CD8+ T-cells in severe COVID-19 patients were less protective. Interestingly, the frequency, memory phenotype, and activation profiles of circulating B15/S919+CD8+ T-cells did not differ across disease severity. Moreover, B15/S919+CD8+ T-cells were better maintained into convalescence compared to other SARS-CoV-2-specificities. Our study thus provides evidence on the differential nature of the TCR clonal repertoire in 22.37% of HLA-B*15:01-positive COVID-19 patients who developed severe or critical disease in our cohorts, comparing to HLA-B*15:01-expressing individuals with mild COVID-19.
Original languageEnglish
Article numbere2503145122
Pages (from-to)1-10
Number of pages10
JournalProceedings of the National Academy of Sciences of the United States of America
Volume122
Issue number36
Early online date2 Sept 2025
DOIs
Publication statusPublished - 9 Sept 2025

Keywords

  • HLA-B*15:01
  • COVID-19
  • T cell receptors
  • Middle aged
  • Aged
  • CD8+ T cells
  • CD8-positive T-lymphocytes - immunology
  • Severe disease
  • Male
  • SARS-CoV-2 - immunology
  • Adult
  • Humans
  • Female
  • COVID-19 - immunology - genetics
  • Spike glycoprotein, Coronavirus - immunology

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