Alan Engelman

This study uses molecular dynamics simulations to show that IN-RNA filaments guide HIV-1 capsid assembly and shape, with octameric filaments forming more conical capsids than tetrameric ones.

The paper introduces HIV SMRTcap, a method for characterizing HIV-1 reservoirs by identifying integration sites and proviral integrity using long-read sequencing, and validates its performance across subtypes and tissue samples.

This study determines cryo-EM structures of HIV-1 integrase tetramers and intasome hexadecamers, revealing structural plasticity and functional roles in viral integration and RNA binding.

This study uses cryo-correlative techniques to analyze HIV-1 nuclear import, revealing dependencies on capsid elasticity, nuclear pore adaptability, and CPSF6 binding.

This study shows that PFV Gag protein interacts with mitotic chromatin, and altered binding affects integration site selection and infectivity.

This paper investigates how the M66I mutation in HIV-1 capsid protein confers resistance to lenacapavir by altering inhibitor binding and viral replication.

This study shows CPSF6 promotes HIV-1 preintegration complex function by enhancing viral DNA integration into gene-dense regions and restoring integration activity when added back to mutant cells.

This study shows that sequential binding of CypA and CPSF6 to HIV-1 capsid is necessary for nuclear entry and integration, and that lenacapavir targets this process.

This study identifies the mechanism by which lenacapavir inhibits HIV-1 maturation by altering capsid protein assembly.

This study shows that the RANBP2-Cyp domain influences HIV-1 infection and MX2 activity by modulating CA interactions with nucleoporins and integration targeting.

This study investigates how the nuclear localization signal (NLS) of CPSF6 influences HIV-1 infection after nuclear import, showing that some NLSs impair viral integration.

The paper shows that disrupting HIV-1 integrase interactions with LEDGF/p75 increases antisense RNA (asRNA) production in HIV-1 infected cells.

This study shows LEDGF is recruited to promoters by MLL1 and recruits RNA Pol II, facilitating HIV-1 integration across gene bodies.