literature

HIV mutation literature information.

Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.

PMID: 19812032 2009 The Journal of biological chemistry

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.

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 M41L, D67N, K70R, L210W, T215F/Y, and K219Q/E/N, which are primary resistance mutations for AZT and stavudine, are called thymidine analog mutations (TAMs), AZTr, or excision-enhancing mutations.

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.

HIV type 1 subtype diversity and drug resistance among HIV type 1-infected Kenyan patients initiating antiretroviral therapy.

PMID: 19954302 2009 AIDS research and human retroviruses

Abstract: Of these patients, three had nucleoside RTI resistance mutations, such as M184V, K65R, D67N, K70R, and K219Q.

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.

AZT resistance of simian foamy virus reverse transcriptase is based on the excision of AZTMP in the presence of ATP.

PMID: 18096624 2008 Nucleic acids research

Discussion: The mutations involved in the enhanced excision of AZTMP in HIV-1 RT are M41L, D67N, K70R, T215Y/F and K219Q/E (Figure 7).

Identification of a novel resistance (E40F) and compensatory (K43E) substitution in HIV-1 reverse transcriptase.

PMID: 18271957 2008 Retrovirology

Introduction: HIV-1 develops these TAMs by two distinct pathways: the TAM-1 pathway consisting of T215Y, M41L, L210W and sometimes D67N or the TAM-2 pathway including T215F, K70R, K21

Discussion: In this study we show that these E40F and K43E changes are highly associated with mutations from the TAM-1 pathway (M41L, L210W and T215Y) and less with the amino acid changes from the TAM-2 pathway (D67N, K70R, T215F and K219Q/E) (Table 2).

Prevalence of genotypic resistance to nucleoside analogues, nonnucleoside analogues, and protease inhibitors in HIV-infected persons in Athens, Greece.

PMID: 18275347 2008 AIDS research and human retroviruses

Abstract: The most frequent ARMs of each drug category were to NRTIs at codons M184V [present in 149 tests (63.6%)], M41L [79 (33.8%)], K70R [66 (28.2%)], M184VI [58 (24.8%)], T215YF [53 (22.7%)], D67N [82 (35.0%)], T215Y [72 (30.8%)], K219Q [47 (20.1%)], K219E/Q [54 (23.1%)], and L210W [49 (20.9%)], respectively.

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%).

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