Jonathan Dias

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.

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 uses humanized mice to compare HIV-1 persistence in liver/lung macrophages and CD4+ T-cells during ART, finding macrophages contribute less to viral reservoirs than T-cells.

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