Pablo Tebas

This study shows antigen stimulation can reactivate HIV-1 proviruses integrated in repressive chromatin, suggesting deeper latency may contribute to viral rebound.

The paper identifies BACH2-driven tissue-resident memory programs in gut CD4+ T cells as a mechanism promoting HIV-1 persistence and suggests BACH2 as a therapeutic target.

This study identifies Retinol Binding Protein 4 (RBP4) as a natural activator of latent HIV-1 through JAK/STAT5 and JNK pathways, offering a new strategy for reactivating viral reservoirs.

The paper shows that cognate antigen engagement in CD4+ T cells on long-term ART increases HIV-1 transcription through T cell activation, suggesting a role in viral rebound.

The paper isolates and characterizes neutralizing anti-interferon-alpha and anti-interferon-beta antibodies from human patients, showing their specificity and potential therapeutic applications.