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Title: Impact of resistance mutations on inhibitor binding to HIV-1 integrase

Journal Article · · Journal of Chemical Information and Modeling
DOI:https://doi.org/10.1021/ci400537n· OSTI ID:1346623
 [1];  [2];  [3];  [4];  [1];  [3];  [1]
  1. Shanghai Jiao Tong Univ., Shanghai (China)
  2. Univ. of Tennessee Health Science Center, Memphis, TN (United States)
  3. Oak Ridge National Lab. (ORNL), Oak Ridge, TN (United States); Univ. of Tennessee, Knoxville, TN (United States)
  4. Logistics College of Chinese People's Armed Police Force, Tianjin (China)

Here, HIV-1 integrase (IN) is essential for HIV-1 replication, catalyzing two key reaction steps termed 3' processing and strand transfer. Therefore, IN has become an important target for antiviral drug discovery. However, mutants have emerged, such as E92Q/N155H and G140S/Q148H, which confer resistance to raltegravir (RAL), the first IN strand transfer inhibitor (INSTI) approved by the FDA, and to the recently approved elvitegravir (EVG). To gain insights into the molecular mechanisms of ligand binding and drug resistance, we performed molecular dynamics (MD) simulations of homology models of the HIV-1 IN and four relevant mutants complexed with viral DNA and RAL. The results show that the structure and dynamics of the 140s loop, comprising residues 140 to 149, are strongly influenced by the IN mutations. In the simulation of the G140S/Q148H double mutant, we observe spontaneous dissociation of RAL from the active site, followed by an intrahelical swing-back of the 3' -OH group of nucleotide A17, consistent with the experimental observation that the G140S/Q148H mutant exhibits the highest resistance to RAL compared to other IN mutants. An important hydrogen bond between residues 145 and 148 is present in the wild-type IN but not in the G140S/Q148H mutant, accounting for the structural and dynamical differences of the 140s' loop and ultimately impairing RAL binding in the double mutant. End-point free energy calculations that broadly capture the experimentally known RAL binding profiles elucidate the contributions of the 140s' loop to RAL binding free energies and suggest possible approaches to overcoming drug resistance.

Research Organization:
Oak Ridge National Lab. (ORNL), Oak Ridge, TN (United States)
Sponsoring Organization:
USDOE
DOE Contract Number:
AC05-00OR22725
OSTI ID:
1346623
Journal Information:
Journal of Chemical Information and Modeling, Vol. 53, Issue 12; ISSN 1549-9596
Publisher:
American Chemical Society
Country of Publication:
United States
Language:
English

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