HIV infection stimulates chronic GC reactions with high levels of atypical MBCs, which have been associated with autoimmune disease.29,53–55 To understand the dynamics of MBC differentiation during HIV infection, we investigated a dataset of bulk BCR sequences from lymph node biopsies of 3 HIV-1 infected donors.29 These donors were clinically estimated to have been infected 4 months to 3 years prior based on the strength and timing of HIV antibody tests (Fig. 4A, donor H1: 12–18mo, H2: 24–36mo, H3: 4–8mo; Dr. Susan Moir, personal communication). Here, BCR is linked to HIV infectious disease.