Multifaceted B-cell response to transient HIV viraemia in elite controllers

Chronic HIV infection drives B-cell dysfunction associated with the accumulation of tissue-like memory (TLMs) and activated memory B cells (MBCs) but decline in resting memory B cells. TLM origin and the mechanisms driving their expansion in HIV infection remain unclear. To elucidate this, we performed single-cell RNA/BCR sequencing of PMBCs enriched for B cells from an elite HIV controller pre-, during and post-viral blip. This provided a new insight into multifaceted functional B-cell response to transient HIV viraemia as likely happens during the early phase of anti-retroviral therapy cessation, highlighting the TLM heterogeneity and the contribution of innate-like B cells which might have important clinical implications for anti-HIV vaccine and therapy design. Overall design: scRNA/BCR/CITE-seq profiling of PBMCs enriched for B cells obtained from an elite HIV controller (no anti-viral treatment) at three different timepoints (pre, during and post viral blip).