A Nature Communications paper revealed that HIV‑infected CD4+ T cells express sialoglycans that inhibit myeloid cell–mediated clearance, allowing infected cells to persist. The study mapped sialoglycan‑mediated interactions and showed that disrupting these glycan signals restored myeloid phagocytosis in vitro. The discovery identifies a glyco‑immune evasion mechanism that could be targeted by glycosylation inhibitors, lectin blockers or antibody designs to enhance myeloid clearance. Vaccine and cure‑strategy researchers can evaluate whether glycan‑targeted interventions augment reservoir reduction approaches.