In 1996, Paul Bieniasz joined Bryan Cullen's lab at
Duke University as a postdoctoral associate. 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 and HIV-1 Tat interaction with
host factors. Bieniasz started his own independent lab in 1999 at the
Aaron Diamond AIDS Research Center and
Rockefeller University in
New York. Initially he worked on understanding how later steps of viral infection, such as assembly and budding, were inhibited in rodent cells. This interest in
viral budding came to define Bieniasz's career. Bieniasz showed that the
retroviral protein Gag assembles at the
plasma membrane, recruiting the viral
genome by hijacking a specialized cellular protein complex involved in
membrane vesicle trafficking, the
ESCRT complex. Together with his wife and colleague,
Theodora Hatziioannou, they identified several host-specific factors that restrict replication of HIV-1 in
macaques.
Tetherin, a potent antiviral factor, was also discovered in his lab and shown to be counteracted by the HIV-1 accessory protein Vpu. 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. 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, and that CG-depletion of HIV-1 genomes is a mechanism to evade the antiviral, RNA-binding protein ZAP. 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. == References ==