Researchers published mechanistic evidence that HIV-infected CD4+ T cells exploit sialoglycans on their surface to resist destruction by myeloid immune cells. The Nature Communications study led by Singh, Islam and Liu maps how altered glycosylation patterns reduce phagocytic clearance and enable infected cells to persist. The team used molecular profiling and functional assays to connect specific sialoglycan structures with impaired myeloid recognition. The finding uncovers a potential therapeutic axis: targeting sialoglycan pathways or employing sialic-acid–binding inhibitors could sensitize reservoirs to immune clearance. This work is preclinical and frames a testable strategy to complement antiretroviral therapy by removing infected cellular reservoirs.