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 HIV mutation literature information.


  High prevalence of genotypic and phenotypic HIV-1 drug-resistant strains among patients receiving antiretroviral therapy in Abidjan, Cote d'Ivoire.
 PMID: 11391173       2001       Journal of acquired immune deficiency syndromes (1999)
Abstract: The prevalence of mutations associated with resistance to ARV drugs was: 29 (42.6%) to zidovudine, 10 (14.7%) to lamivudine, one (1.5%) to didanosine, one K103N mutation (associated with resistance to delavirdine, nevirapine, and efavirenz), one Y181C mutation (associated with resistance to delavirdine and nevirapine), two to both indinavir (M46I/L and V82A) and saquinavir (G48V and L90M), and one each to ritonavir (V82A) and nelfinavir (D30N).


  Resistance profiles to antiretroviral drugs in HIV-1 drug-naive patients in Argentina.
 PMID: 11417764       2001       Antiviral therapy
Abstract: In the viral protease region, 1/86 (1.2%) individuals carried the D30N mutation, whereas 1/85 (1.2%) had the M41L mutation in the reverse transcriptase (RT) region.


  Resistance-associated mutations in the human immunodeficiency virus type 1 subtype c protease gene from treated and untreated patients in the United Kingdom.
 PMID: 11427587       2001       Journal of clinical microbiology
Abstract: D30N, M46I, V82A/F, and I84V were seen rarely.


  Replicative fitness in vivo of HIV-1 variants with multiple drug resistance-associated mutations.
 PMID: 11536226       2001       Journal of medical virology
Abstract: The least fit viruses were associated with the RT mutation M184I/V (11.6% less fit) and the PR mutations D30N (12.4% less fit) and M46I/L (21% less fit).


  DPC 681 and DPC 684: potent, selective inhibitors of human immunodeficiency virus protease active against clinically relevant mutant variants.
 PMID: 11600351       2001       Antimicrobial agents and chemotherapy
Abstract: DPC 681 and DPC 684 showed no loss in potency toward recombinant mutant HIVs with the D30N mutation and a fivefold or smaller loss in potency toward mutant variants with three to five amino acid substitutions.


  Emergence of drug resistance mutations in a group of HIV-infected children taking nelfinavir-containing regimens.
 PMID: 11602042       2001       AIDS research and human retroviruses
Abstract: PI resistance mutations occurred in eight patients: D30N in six, and L90M in three.


  Nelfinavir: an update on its use in HIV infection.
 PMID: 10776836       2000       Drugs
Abstract: Nelfinavir primarily selects for the D30N mutation, which is not seen with other protease inhibitors, and alone does not cause resistance to other protease inhibitors in vitro.


  Prevalence of drug resistant mutants and virological response to combination therapy in patients with primary HIV-1 infection.
 PMID: 10797372       2000       Journal of medical virology
Abstract: Two percent (1/48) had a major mutation associated with resistance to protease inhibitors (D30N).


  Correlation between human immunodeficiency virus genotypic resistance and virologic response in patients receiving nelfinavir monotherapy or nelfinavir with lamivudine and zidovudine.
 PMID: 10915071       2000       The Journal of infectious diseases
Abstract: M184V preceded D30N in all determinable instances.
Abstract: All 6 PR-RT(+) patients had virus with M184V (lamuvidine resistance); 3 isolates also contained D30N (nelfinavir resistance).


  Replicative fitness of protease inhibitor-resistant mutants of human immunodeficiency virus type 1.
 PMID: 10196268       1999       Journal of virology
Abstract: A major natural polymorphism of the HIV-1 protease, L63P, compensated well for the impairment of fitness caused by L90M but only slightly improved the fitness of D30N.
Abstract: A nelfinavir-selected protease D30N substitution substantially decreased replicative capacity relative to WT, while a saquinavir-selected L90M substitution moderately decreased fitness.
Abstract: Hypotheses based on the greater fitness impairment of the nelfinavir-selected D30N mutant are suggested to explain observations that prolonged responses to delayed salvage regimens, including alternate PIs, may be relatively common after nelfinavir failure.



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