Premature skewing of T cell receptor clonality and delayed memory expansion in HIV-exposed infants

Sonwabile Dzanibe, Aaron J. Wilk, Susan Canny, Thanmayi Ranganath, Berenice Alinde, Florian Rubelt, Huang Huang, Mark M. Davis, Susan P. Holmes, Heather B. Jaspan (), Catherine A. Blish () and Clive M. Gray ()
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Sonwabile Dzanibe: University of Cape Town
Aaron J. Wilk: Stanford University
Susan Canny: Stanford University
Thanmayi Ranganath: Stanford University
Berenice Alinde: Stellenbosch University
Florian Rubelt: Stanford University School of Medicine
Huang Huang: Stanford University School of Medicine
Mark M. Davis: Stanford University School of Medicine
Susan P. Holmes: Stanford University
Heather B. Jaspan: University of Cape Town
Catherine A. Blish: Stanford University
Clive M. Gray: University of Cape Town

Nature Communications, 2024, vol. 15, issue 1, 1-15

Abstract: Abstract While preventing vertical HIV transmission has been very successful, HIV-exposed uninfected infants (iHEU) experience an elevated risk to infections compared to HIV-unexposed and uninfected infants (iHUU). Here we present a longitudinal multimodal analysis of infant immune ontogeny that highlights the impact of HIV/ARV exposure. Using mass cytometry, we show alterations in T cell memory differentiation between iHEU and iHUU being significant from week 15 of life. The altered memory T cell differentiation in iHEU was preceded by lower TCR Vβ clonotypic diversity and linked to TCR clonal depletion within the naïve T cell compartment. Compared to iHUU, iHEU had elevated CD56loCD16loPerforin+CD38+CD45RA+FcεRIγ+ NK cells at 1 month postpartum and whose abundance pre-vaccination were predictive of vaccine-induced pertussis and rotavirus antibody responses post 3 months of life. Collectively, HIV/ARV exposure disrupted the trajectory of innate and adaptive immunity from birth which may underlie relative vulnerability to infections in iHEU.

Date: 2024
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DOI: 10.1038/s41467-024-47955-5

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