A Nature Communications study revealed that HIV‑infected CD4+ T cells upregulate sialoglycans on their surfaces to avoid phagocytic destruction by myeloid cells. The authors mapped the glycan modifications and showed how they impair innate immune recognition, enabling infected cells to persist. Sialoglycans are complex cell‑surface sugars that modulate immune interactions; the paper links glycosylation changes to viral immune evasion and suggests therapeutic entry points such as glycan‑editing enzymes or glycan‑blocking antibodies. Findings are relevant for cure‑oriented strategies that aim to expose and eliminate persistent HIV reservoirs.