Dual HLA B*42 and B*81-reactive T cell receptors recognize more diverse HIV-1 Gag escape variants

Funsho Ogunshola, Gursev Anmole, Rachel L. Miller, Emily Goering, Thandeka Nkosi, Daniel Muema, Jaclyn Mann, Nasreen Ismail, Denis Chopera, Thumbi Ndung’u, Mark A. Brockman () and Zaza M Ndhlovu ()
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Funsho Ogunshola: University of KwaZulu-Natal
Gursev Anmole: Simon Fraser University
Rachel L. Miller: Simon Fraser University
Emily Goering: Ragon Institute of MGH, MIT, and Harvard
Thandeka Nkosi: University of KwaZulu-Natal
Daniel Muema: University of KwaZulu-Natal
Jaclyn Mann: University of KwaZulu-Natal
Nasreen Ismail: University of KwaZulu-Natal
Denis Chopera: University of KwaZulu-Natal
Thumbi Ndung’u: University of KwaZulu-Natal
Mark A. Brockman: Simon Fraser University
Zaza M Ndhlovu: University of KwaZulu-Natal

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Some closely related human leukocyte antigen (HLA) alleles are associated with variable clinical outcomes following HIV-1 infection despite presenting the same viral epitopes. Mechanisms underlying these differences remain unclear but may be due to intrinsic characteristics of the HLA alleles or responding T cell repertoires. Here we examine CD8+ T cell responses against the immunodominant HIV-1 Gag epitope TL9 (TPQDLNTML180–188) in the context of the protective allele B*81:01 and the less protective allele B*42:01. We observe a population of dual-reactive T cells that recognize TL9 presented by both B*81:01 and B*42:01 in individuals lacking one allele. The presence of dual-reactive T cells is associated with lower plasma viremia, suggesting a clinical benefit. In B*42:01 expressing individuals, the dual-reactive phenotype defines public T cell receptor (TCR) clones that recognize a wider range of TL9 escape variants, consistent with enhanced control of viral infection through containment of HIV-1 sequence adaptation.

Date: 2018
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DOI: 10.1038/s41467-018-07209-7

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