A. Saez-Cirion

This study uses mathematical modeling of SIV-infected macaques to show that early CD8 T-cell suppressive capacity predicts natural control of infection.

This study shows HIV-1 spreads between T lymphocytes via extracellular matrix (ECM)-clustered viral particles, enhancing transmission efficiency and resistance to antiretroviral treatment and antibodies.

This study identifies UHRF1 as a novel mediator of HIV-1 latency through DNA methylation and shows its inhibition reactivates latent HIV-1 in patient cells.

The paper shows that AAC-11-derived peptides induce death of HIV-1 susceptible CD4+ T cells by targeting metabolically active cells.

Modeling SIV dynamics in natural controller macaques shows viral control is driven by early cytotoxic T-cell response and reveals distinct infected cell compartments with different turnover rates.

This study shows that optimal maturation of SIV-specific CD8+ T-cells correlates with natural control of SIV infection in macaques, with controllers developing more potent antiviral responses over time.