HIV mutation literature information.


  Detection of Gag C-terminal mutations among HIV-1 non-B subtypes in a subset of Cameroonian patients.
 PMID: 35082353       2022       Scientific reports
Introduction: Following the Stanford algorithm (mutation list), minor resistance mutations (L10F, V11I, K20TV, L23I, L33F, K43T, F53L, Q58E, A71IL, G73STCA, T74P, N83D, and L89V) are assumed to have ancillary roles such as compensation for lower efficiency of proteolysis caused by major mutations; major resistance mutations (V32I, M46IL, I47VA, G48VM,  PMID: 29124158       2015       Biochemistry and biophysics reports
Introduction: Clinical isolates previously obtained from the Wayne State University Infectious Disease Clinic in Detroit, MI contain major drug resistance mutations L33F, I47V, I50V, I54M, L76V, V82I/F, and I84F as well as nonpolymorphicaccessory mutations L10V/G, V11I, I13V, K20T/R, L33I/M, K43T, F53L, A71L, T74P, and L89V.


  HIV-1 transmitted drug resistance-associated mutations and mutation co-variation in HIV-1 treatment-naive MSM from 2011 to 2013 in Beijing, China.
 PMID: 25510523       2014       BMC infectious diseases
Abstract: Fifty-seven samples had at least one TDR-associated mutation, mainly including L10I/V (6.3%), A71L/T/V (6.3%), V179D/E (5.4%), and V106I (2.7%), with different distributions of TDR-associated mutations by different HIV-1 subtypes and by each year.
Result: PI mutations included L10I/V (7.2%, 16/223) and A71L/T/V (6.3%, 14/223), with relatively high frequency; NRTI mutations, included L74I (0.45%, 1/223) and V75L (0.45%, 1/223); and the most frequent NNRTI mutation was V179D/E (5.4%, 12/223).
Table:


  The role of mutations at codons 32, 47, 54, and 90 in HIV-1 protease flap dynamics.
 PMID: 32309558       2014       Discoveries (Craiova, Romania)
Introduction: The DetMDRs also contain previously identified non-polymorphic accessory mutations L10V/G, V11I, I13V, K20T/R, L33F/I/M, K43T, F53L, A71L, T74P, and L89V.


  Low frequency of genotypic resistance in HIV-1-infected patients failing an atazanavir-containing regimen: a clinical cohort study.
 PMID: 23711895       2013       The Journal of antimicrobial chemotherapy
Result: The remaining 43 minor atazanavir mutations were either not detected in this dataset (L10C, K20V, E34Q, F53Y, I54L/M/T/A, A71L, G73C/T, V82F and I93M) or were not significantly associated with atazanavir exposure (L10I/F/V, G16E, K20R/M/I/T, L24I, V32I, L33I/F/V, M36L/V, M46L, G48V, I54V


  Interpretation of genotype and pharmacokinetics for resistance to fosamprenavir-ritonavir-based regimens in antiretroviral-experienced patients.
 PMID: 17296739       2007       Antimicrobial agents and chemotherapy
Abstract: The Zephir mutation score included 12 IAS protease mutations associated with poorer virological response: L10I/F/R/V, L33F, M36I, M46I/L, I54L/M/T/V, I62V, L63P, A71I/L/V/T, G73A/C/F/T, V82A/F/S/T, I84V, L90M, and polymorphism mutations I13V, L19I, K55R, and L89M.


  Virological responses to atazanavir-ritonavir-based regimens: resistance-substitutions score and pharmacokinetic parameters (Reyaphar study).
 PMID: 16856615       2006       Antiviral therapy
Abstract: The Reyaphar score included 12 baseline protease substitutions from the International AIDS Society USA list that were associated with poorer VR: L10I/F/R/V, K20I/M/R, L241, M461/L, 154L/M/T/V, L63P, A71I/L/V/T, G73A/C/F/T, V771, V82A/F/S/T, 184V, L90M and the polymorphism substitution Q58E.


  Identification of genotypic changes in human immunodeficiency virus protease that correlate with reduced susceptibility to the protease inhibitor lopinavir among viral isolates from protease inhibitor-experienced patients.
 PMID: 11462018       2001       Journal of virology
Abstract: Two statistical tests showed that specific mutations at 11 amino acid positions in protease (L10F/I/R/V, K20M/R, L24I, M46I/L, F53L, I54L/T/V, L63P, A71I/L/T/V, V82A/F/T, I84V, and L90M) were associated with reduced susceptibility.



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