At Duke, Bieniasz studied several aspects of the HIV-1 life cycle, including the determinants of specificity in the viral envelope with the cellular receptor CCR5[6] and HIV-1 Tat interaction with host factors.
[7] Bieniasz started his own independent lab in 1999 at the Aaron Diamond AIDS Research Center and Rockefeller University in New York.
[12] Subsequently, another inhibitor of HIV-1 replication was discovered in his lab, Mx2, a cellular protein shown to inhibit post-entry steps of the HIV-1 infection.
[13] In recent years, Paul Bieniasz's group has focused on viral RNA interactions with cellular proteins; in particular, his group showed that APOBEC3G is recruited to virions by interaction with the viral RNA,[14][15] and that CG-depletion of HIV-1 genomes is a mechanism to evade the antiviral, RNA-binding protein ZAP.
[16] Bieniasz acted as Chair of the NIH AIDS Molecular and Cellular Biology study section from 2004 to 2009 and served on the NCI Board of Scientific Counselors from 2010 to 2014.