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 HIV mutation literature information.


  Primary HIV-1 drug resistance and polymorphic patterns among injecting drug users (IDUs) in Chennai, Southern India.
 PMID: 19721100       2009       Journal of the International Association of Physicians in AIDS Care (Chicago, Ill.
Abstract: RESULTS: M41LM (1.8%), K65KN (1.8%), and G73GS (2.7%) were found to be associated with low-level resistance to zidovudine (ZDV), stavudine (d4T), abacavir (ABC), didanosine (ddI), emtricitabine (FTC), tenofovir (TDF), and saquinavir (SQV) in each specimen.


  Thymidine analogue resistance suppression by V75I of HIV-1 reverse transcriptase: effects of substituting valine 75 on stavudine excision and discrimination.
 PMID: 19801659       2009       The Journal of biological chemistry
Abstract: M41L/A62V/T69SSS/K70R/T215Y), the introduction of V75I led to a significant decrease of its ATP-dependent excision activity on AZT-, d4T-, and acyclovir-terminated primers.
Abstract: Recombinant HIV-1 containing the M41L/A62V/T69SSS/K70R/V75I/T215Y RT showed 18.3- and 1.5-fold increased susceptibility to AZT and d4T, respectively, in comparison with virus containing the M41L/A62V/T69SSS/K70R


  Structural basis for the role of the K65R mutation in HIV-1 reverse transcriptase polymerization, excision antagonism, and tenofovir resistance.
 PMID: 19812032       2009       The Journal of biological chemistry
Introduction: Mutations
Figure: Superposition of excision-enhancing mutation or TAM (M41L, D67N, K70R, T215Y, and K219Q) RT dsDNA AZTppppA structure4 on K65R RT dsDNA dATP structure at their dNTP-binding sites; AZTppppA is the product of AZT monophosphate by ATP-mediated excision.
Discussion: TAMs (M41L, D67N, K70R, T215Y/F, and K219Q/E/N) cause enhanced NRTI excision, a major mechanism of resistance where the excision of incorporated nucleotides is mediated by ATP.


  RT-SHIV subpopulation dynamics in infected macaques during anti-HIV therapy.
 PMID: 19889213       2009       Retrovirology
Discussion: The 214F mutation is associated with nucleoside analogue mutation cluster 2 (D67N+K70R+K219Q+T215F) and negatively associated with nucleotide analogue mutation cluster 1 (M41L+L210W+T215Y).


  Viremia, resuppression, and time to resistance in human immunodeficiency virus (HIV) subtype C during first-line antiretroviral therapy in South Africa.
 PMID: 19911963       2009       Clinical infectious diseases
Method: Thymidine associated mutations (TAMs) were M41L, D67N, K70R, L210W, T215Y/F, K219Q/E and multi-NRTI mutations included TAMS, K65R, and L74V.


  Genotypic HIV type-1 drug resistance among patients with immunological failure to first-line antiretroviral therapy in south India.
 PMID: 19918105       2009       Antiviral therapy
Result: In total, 63% in group A and 74% in group B had thymidine analogue mutations (TAMs), with M41L and T215Y significantly (P<0.05) higher in group B (Table 2).
Discussion: T215Y, L210W and M41L, which constitute the TAM-1 pathway were significantly higher in group B, and this might be associated with their prior AZT/3TC dual therapy prior to HAART.


  Antiretroviral genotypic resistance mutations in HIV-1 infected Korean patients with virologic failure.
 PMID: 19949656       2009       Journal of Korean medical science
Result: M41L, I54V, D30N, and V82A/T/S were observed in more than 10 patients and K103N (10/41, 24.4%) was the most frequently observed NNRTI associated mutation.


  Treatment outcomes and plasma level of ritonavir-boosted lopinavir monotherapy among HIV-infected patients who had NRTI and NNRTI failure.
 PMID: 20030841       2009       AIDS research and therapy
Result: The frequencies of thymidine analogue associated mutations (TAMs) were 17 (43%) D67N, 16 (40%) T215FY, 8 (20%) M41L, 6 (15%) K60R, 6 (15%) L210W, 2 (5%) K219Q.


  The K65R mutation in HIV-1 reverse transcriptase: genetic barriers, resistance profile and clinical implications.
 PMID: 20190870       2009       HIV therapy
Introduction: Two distinct TAM (TAM-1 and -2) pathways lead to the stepwise accumulation of major (M41L, K70R and T215Y/F), minor/secondary (D67N and L210W) and compensatory (E44D, V118I and H208Y) mutations that confer a 5-500-fold reduced susceptibility to AZT and broad cross-resistance between NRTIs (Figure 1).


  Mechanisms by which the G333D mutation in human immunodeficiency virus type 1 Reverse transcriptase facilitates dual resistance to zidovudine and lamivudine.
 PMID: 17967907       2008       Antimicrobial agents and chemotherapy
Abstract: To provide insight into the biochemical mechanism(s) involved, we investigated the effect of the G333D mutation in the connection domain of RT on resistance to zidovudine (AZT) and lamivudine (3TC) in enzymes that contain both M184V and thymidine analog mutations (TAMs; M41L, L210W, and T215Y).



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