HIV mutation literature information.


  Structural characterization of B and non-B subtypes of HIV-protease: insights into the natural susceptibility to drug resistance development.
 PMID: 17467738       2007       Journal of molecular biology
Abstract: Our results further indicate that two naturally occurring polymorphic substitutions in subtype F and other non-B HIV proteases, M36I and L89M, may lead to early development of drug resistance in patients infected with non-B HIV subtypes.
Abstract: We have also solved crystal structures of two multi-drug resistant mutant HIV PRs in complex with TL-3, from subtype B (Bmut) carrying the primary mutations V82A and L90M, and from subtype F (Fmut) carrying the primary mutation V82A plus the secondary mutation M36I, at 1.75 A and 2.8 A resolution, respectively.


  Effective program against mother-to-child transmission of HIV at Saint Camille Medical Centre in Burkina Faso.
 PMID: 17516517       2007       Journal of medical virology
Abstract: All children had recombinant HIV-1 strain (CRF06_CPX) with: minor PR mutations (M36I, K20I) and RT mutations (R211K).


  Computational characterization of structural role of the non-active site mutation M36I of human immunodeficiency virus type 1 protease.
 PMID: 17524421       2007       Journal of molecular biology
Abstract: M36I is the most frequently observed polymorphism in non-subtype B HIV-1 proteases.
Abstract: Here, we performed molecular dynamics (MD) simulations of M36I protease in complex with nelfinavir and revealed the influence of the M36I mutation.
Abstract: However, since the 36th residue is located at a non-active site of the protease and has no direct interaction with any ligands, the structural role of M36I remains unclear.


  Polymorphisms and drug resistance analysis of HIV-1 CRF01_AE strains circulating in Fujian Province, China.
 PMID: 17619115       2007       Archives of virology
Abstract: RESULTS: In comparison with the consensus sequence of B strains, the most common protease polymorphisms in HIV-1 CRF01_AE strains prevailing in Fujian Province, China, were I13V (76.9%), E35D (76.9%), M36I (100%), R41K (98.1%), H69K (90.4%), and L89M (96.2%).
Abstract: The proportion of substitutions L63P, A71T/V, V77I and I93L in subtype B' sequences was considerably higher than in CRF01_AE viruses, while the proportion of L10I, M36I and K20R/I substitutions in subtype B' sequences was relativ


  Genotypic resistance mutations in treatment-naive and treatment-experienced patients under widespread use of antiretroviral drugs in Thailand: implications for further epidemiologic surveillance.
 PMID: 17881868       2007       Japanese journal of infectious diseases
Abstract: The most commonly found marker in drug-naive patients was M36I/V/L (n=90, 81.1%), which is a common natural polymorphism among HIV-1 subtype CRF01_AE individuals.


  Genotypic and phenotypic analyses of human immunodeficiency virus type 1 in antiretroviral drug-naive Nigerian patients.
 PMID: 16438641       2006       AIDS research and human retroviruses
Abstract: Within the protease region, all 18 isolates had mutations/polymorphic substitutions at six locations compared to the HIV-1 NL4-3 reference sequence, two of which have been associated with resistance to protease inhibitors (K20I and M36I).


  Short communication: low prevalence of genotypic drug resistance mutations among antiretroviral-naive HIV type 1 patients in Malaysia.
 PMID: 16478392       2006       AIDS research and human retroviruses
Abstract: Amino acid substitutions I13V, E35D, and M36I were associated with CRF01_AE while L63P, V77I, and I93L were associated with subtype B.


  Effects of drug resistance on viral load in patients failing antiretroviral therapy.
 PMID: 16555280       2006       Journal of medical virology
Abstract: Certain reverse transcriptase mutations such as M184V/I, K70R, V108I, and protease mutations such as L33FIV, M84V, and M36I were associated with reduced viral load.


  Natural polymorphisms in the protease gene modulate the replicative capacity of non-B HIV-1 variants in the absence of drug pressure.
 PMID: 16765636       2006       Journal of clinical virology
Abstract: All but one drug-naive individual carrying non-B viruses were fully susceptibility to all tested PI, suggesting that additional substitutions within the PR might compensate the reduced PI susceptibility caused by K20I and/or M36I.
Abstract: OBJECTIVE: To evaluate the effect of two natural protease (PR) polymorphisms, K20I and M36I, which are frequently found in non-B subtypes, on the virus replicative capacity in the presence and absence of protease inhibitors (PI).
Abstract: RESULTS: In the absence of drug, the M36I clone replicated more rapidly than wt (wi


  Diversity of HIV in rural Burkina Faso.
 PMID: 16951652       2006       Journal of acquired immune deficiency syndromes (1999)
Abstract: Resistance-associated polymorphisms (K20I and M36I) were prevalent in the complete protease (PR) region, but no primary drug resistance mutations were detected.



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