Abstract
HIV controllers can control viral replication and remain healthy, but the mechanism behind this control is unknown. Despite human leukocyte antigen (HLA) diversity in the population, almost 50% of HIV controllers express the HLA-B∗57:01 molecule, which presents, among others, the Gag-derived epitope TW10. Given TW10's presentation in early infection, TW10-specific Tcells could participate in the control of HIV. Here, we study the strength and functionality of TW10-specific Tcells from HLA-B∗57:01+/HIV+ controller and non-controller individuals. We determine the TW10-specific Tcell receptor (TCR) repertoire, revealing a bias in TCR gene usage with the presence of a public TCR. We determine that the Tcell response is polyfunctional regardless of the viral load, despite the low affinity of TW10-specific TCRs. We solve the crystal structure of HLA-B∗57:01-TW10 in complex with a TCR, providing the basis of recognition that underpins the strong TRBV5 bias observed in TW10-specific clonotypes.
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