Document Detail


Understanding the HIV-1 protease nelfinavir resistance mutation D30N in subtypes B and C through molecular dynamics simulations.
MedLine Citation:
PMID:  20541446     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A major concern in the antiretroviral (ARV) treatment of HIV infections with protease inhibitors (PI) is the emergence of resistance, which results from the selection of distinct mutations within the viral protease (PR) gene. Among patients who do not respond to treatment with the PI nelfinavir (NFV), the D30N mutation is often observed. However, several reports have shown that D30N emerges with different frequencies in distinct HIV-1 genetic forms or subtypes. In the present work, we analyzed the binding of NFV and the Gag substrate CA/p2 to PR from HIV-1 subtypes B and C through molecular dynamics (MD) simulations. The wild-type and drug-resistant D30N mutants were investigated in both subtypes. The compensatory mutations N83T and N88D, observed in vitro and in vivo when subtype C acquires D30N, were also studied. D30N appears to facilitate conformational changes in subtype B PR, but not in that from subtype C, and this could be associated with disestablishment of an alpha-helical region of the PR. Furthermore, the total contact areas of NFV or the CA/p2 substrate with the mutant PR correlated with changes in the resistance patterns and replicative capacity. Finally, we observed in our MD simulations that mutant PR proteins show different patterns for hydrophobic/van der Waals contact. These findings suggest that different molecular mechanisms contribute to resistance, and we propose that a single mutation has distinct impacts on different HIV-1 subtypes.
Authors:
Rosemberg O Soares; Paulo R Batista; Mauricio G S Costa; Laurent E Dardenne; Pedro G Pascutti; Marcelo A Soares
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-11
Journal Detail:
Title:  Journal of molecular graphics & modelling     Volume:  29     ISSN:  1873-4243     ISO Abbreviation:  J. Mol. Graph. Model.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-06     Completed Date:  2010-12-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9716237     Medline TA:  J Mol Graph Model     Country:  United States    
Other Details:
Languages:  eng     Pagination:  137-47     Citation Subset:  IM    
Copyright Information:
(c) 2010 Elsevier Inc. All rights reserved.
Affiliation:
Laboratório Nacional de Computação Científica, Petrópolis, Brazil.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Binding Sites
Drug Resistance, Viral / drug effects,  genetics*
HIV Protease / chemistry,  genetics*
HIV Protease Inhibitors / pharmacology*
HIV-1 / classification,  drug effects,  genetics*
Humans
Hydrogen Bonding / drug effects
Hydrophobic and Hydrophilic Interactions / drug effects
Ligands
Molecular Dynamics Simulation*
Molecular Sequence Data
Mutation / genetics*
Nelfinavir / pharmacology*
Protein Structure, Secondary
Substrate Specificity / drug effects
Surface Properties / drug effects
Thermodynamics
Chemical
Reg. No./Substance:
0/HIV Protease Inhibitors; 0/Ligands; 159989-64-7/Nelfinavir; EC 3.4.23.-/HIV Protease; EC 3.4.23.-/p16 protease, Human immunodeficiency virus 1

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