"A Northwestern Medicine study published in Nature Communications has revealed how HIV can protect infected cells by altering the sugars on their surface, hindering the host immune system and avoiding detection. The study also lays the foundations for a new therapeutic approach that could strengthen the fight against the virus, said study senior author Mohamed Abdel-Mohsen, PhD, the Margaret Gray Morton Professor of Medicine in the Division of Infectious Diseases."
"In the study, Adbel-Mohsen and his collaborators used advanced glycomic analysis and gene-editing techniques to show that HIV infection reprograms the glycosylation machinery of infected cells, surface sialic acid-containing glycans (sialoglycans) on infected cells and effectively "cloaking" them. These sialoglycans engage inhibitory Siglec receptors, a family of glycan-binding receptors on immune cells that function as "glyco-immune checkpoints." This interaction suppresses immune cells from fighting the virus, allowing HIV to escape immune surveillance."
HIV infection reprograms infected cells' glycosylation machinery, increasing surface sialic acid-containing glycans (sialoglycans) that cloak infected cells. These sialoglycans engage inhibitory Siglec receptors on immune cells, acting as glyco-immune checkpoints and suppressing immune responses. Antiretroviral therapy suppresses replication but does not eliminate hidden infected cells that can rebound after treatment stops. An experimental therapy pairs an HIV-specific antibody with sialidase to target infected cells, remove excess sialoglycans, and enhance immune-mediated killing while sparing uninfected cells. In cultured cells and mice, antibody-directed sialidase significantly increased immune clearance of infected cells, suggesting a potential therapeutic avenue to reduce reservoirs.
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