Jean‐Pierre Routy

The paper links ALDH activity in monocytes to subclinical coronary atherosclerosis in HIV-1 treated individuals, independent of traditional risk factors.

This study shows that inhibiting REV-ERBβ increases HIV-1 reactivation in CD4+ T-cells but limits virion spread.

This study identifies KLF16 as a repressive transcription factor that inhibits HIV-1 transcription by competing with Sp1 and recruiting repressive complexes.

This study shows that continuous ART causes senescence-like changes in alveolar macrophages, increasing inflammation and impairing immune responses to SARS-CoV-2.

The paper identifies specific T-cell subsets with gut-homing/residency markers that predict HIV status and subclinical atherosclerosis in ART-treated individuals.

This study identifies RIG-I deficiency as a cause of classic Kaposi sarcoma by impairing control of KSHV infection and reactivation.

The paper examines immunosenescence trajectories in diverse populations, finding associations between immunological age and brain atrophy, while highlighting CMV status and genetic ancestry as key factors.

This study shows metformin reduces HIV-1 virion release and increases antibody recognition of infected CD4+ T-cells by modulating BST2 and Bcl-2 expression in HIV-positive individuals on ART.

This study shows retinoic acid enhances R5 HIV-1 replication in macrophages through CCR5/SAMHD1 and mTOR pathways.

This study identifies immunological markers associated with subclinical coronary artery atherosclerosis in HIV+ individuals on ART, finding reduced Th17/Treg ratios and increased non-classical monocyte frequencies correlate with atherosclerosis burden.

The paper investigates how HIV and antiretroviral therapy affect the transcriptional and epigenetic response of alveolar macrophages to Mycobacterium tuberculosis.