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 HIV mutation literature information.


  Discordant genotypic interpretation and phenotypic role of protease mutations in HIV-1 subtypes B and G.
 PMID: 19136678       2009       The Journal of antimicrobial chemotherapy
Abstract: Indinavir-associated mutations M46I/L, I84V and V82A/F/T developed earlier in subtype B across the time of exposure to that drug when compared with subtype G counterparts.


  Distinct resistance mutation and polymorphism acquisition in HIV-1 protease of subtypes B and F1 from children and adult patients under virological failure.
 PMID: 18992847       2009       Infection, genetics and evolution
Meth
Result: Ninety-seven percent of isolates with V82A/F/T/S mutations were from patients treated with IDV, RTV and/or LPV, and 89% of those with L90M were from patients treated with NFV and/or SQV.
Table: V82F


  Active-site mutations in the South african human immunodeficiency virus type 1 subtype C protease have a significant impact on clinical inhibitor binding: kinetic and thermodynamic study.
 PMID: 18768960       2008       Journal of virology
Abstract: Study of active-site mutations (the V82A single mutation and the V82F I84V double mutation) in the less-studied South African HIV type 1 subtype C (C-SA) protease indicated that neither mutation had a significant impact on the proteolytic functioning of the protease.
Abstract: Therefore, our results show that the C-SA V82F I84V double mutation decreased the binding affinities of protease inhibitors to levels significantly lower than that required for effective inhibition.


  Comparative studies on inhibitors of HIV protease: a target for drug design.
 PMID: 19374129       2008       In silico biology
Abstract: The HIV protease-nelfinavir complex (PDB code: 1OHR) and HIV protease V82F/I84V double mutant-tipranavir complex (PDB code: 1D4S) were used as templates for introducing mutations on the HIV protease active site.


  Population trends in the prevalence and patterns of protease resistance related to exposure to unboosted and boosted protease inhibitors.
 PMID: 18839778       2008       Antiviral therapy
Abstract: Individual mutations L33F, M461/L, V82A/F/T/S/L and 184V became relatively more frequent over the period of study.


  HIV drug resistance pattern among HAART-exposed patients with suboptimal virological response in Ouagadougou, Burkina Faso.
 PMID: 18667925       2008       Journal of acquired immune deficiency syndromes (1999)
Abstract: Dominant mutations included M46I (37%), 154V (26%), V82A/T/F (30%) in PR; K103N (44%), G190A/S (16%) and T215F/Y (48%) (NRTIs) in RT.
Abstract: Some resistance mutations, notably D67N/G, K70R and L210W (thymidine analogue mutations-TAMs); K101E, V179E in RT, 154V, V82A/T/F and L90M in PR were significantly higher among CRF06_cpx than CRF02_AG strains (P


  Genotypic resistance profile and clinical progression of treatment-experienced HIV type 1-infected patients with virological failure.
 PMID: 18240962       2008       AIDS research and human retroviruses
Abstract: In multivariable models adjusting for prior AIDS, baseline CD4 counts, HIV-1 RNA, and calendar year, viral resistance variables associated with increased hazards of clinical progression were the presence of reverse transcriptase substitution T215F (p = 0.002) and the presence of three or more protease substitutions among L33F/I/V, V82A/F/L/T, I84V, and L90M (p = 0.003).


  The HIV-1 protease substitution K55R: a protease-inhibitor-associated substitution involved in restoring viral replication.
 PMID: 18252693       2008       The Journal of antimicrobial chemotherapy
Abstract: RESULTS: The K55R mutation, which is not a natural polymorphism, was identified to be strongly associated with protease mutations M46I/L and to a lesser extent L24I, I54V and V82A/T/S/F.


  HIV type 1 pol gene diversity and antiretroviral drug resistance mutations in Santos, Brazil.
 PMID: 18327988       2008       AIDS research and human retroviruses
Abstract: Drug resistance mutations identified in common to subtypes B, F, and recombinants B/F were protease inhibitors M46I/L (29%), I54V (24%), A71V (22%), and V82A/F (31%); reverse transcriptase nucleoside resistance mutations M41L (52%), D67N (30%), K70R (26%), M184V (88%), L210W (29%), T215Y/I/F (65%), and K219Q/E/N (28%); and reverse transcriptase nonnucleoside resistance mutation K103N (52%).


  Clinically validated mutation scores for HIV-1 resistance to fosamprenavir/ritonavir.
 PMID: 18390885       2008       The Journal of antimicrobial chemotherapy
Abstract: Two fosamprenavir/ritonavir mutation scores were constructed: score A (L10F/I/V + L33F + M36I + I54L/M/V/A/T/S + I62V + V82A/F/C/G + I84V + L90M) was based only on mutations associated with a worse VR, whereas score B (L10FIV + L33F + M36I + I54L/M/V/A/T/S + A71V - V77I - N88S + L90M) also took into account favourable mutations.



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