literature

HIV mutation literature information.

Clinical and genotypic findings in HIV-infected patients with the K65R mutation failing first-line antiretroviral therapy in Nigeria.

PMID: 19644383 2009 Journal of acquired immune deficiency syndromes (1999)

Result: Among 21 patients primarily on TDF containing ART, the following mutations were observed: M184V, M184I, S68G, A62V and Y115F and K219E.

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.

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.

The K65R mutation in HIV-1 reverse transcriptase: genetic barriers, resistance profile and clinical implications.

PMID: 20190870 2009 HIV therapy

Introduction: The development of K65R and Q151M may be facilitated for HIV-2 variants originating from West Africa (Senegal and Portugal), harboring NNRTI mutations (K101A, V106I, V179I, Y181I, Y188L and G190A) and TAMs/NAMs (T69N, V75I, V118I, L210N, T215S and K219E) as natural polymorphisms.

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%).

Factors associated with the emergence of K65R in patients with HIV-1 infection treated with combination antiretroviral therapy containing tenofovir.

PMID: 18444871 2008 Clinical infectious diseases

Abstract: RESULTS: In an adjusted logistic regression, TDF treatment with nonnucleoside reverse-transcriptase inhibitors and/or didanosine was associated with the emergence of K65R, whereas the presence of any of the thymidine analogue mutations D67N, K70R, T215F, or K219E/Q was protective.

Connection domain mutations N348I and A360V in HIV-1 reverse transcriptase enhance resistance to 3'-azido-3'-deoxythymidine through both RNase H-dependent and -independent mechanisms.

PMID: 18547911 2008 The Journal of biological chemistry

Introduction: This region includes polymerase domain mutations M41L, D67N, K70R, L210W, T215F/Y, and K219Q/E, which are referred to as thymidine analogue-associated mutations (TAMs).

Result: Furthermore, A360V was highly correlated with various mutations considered to be part of the TAMs cluster; for example, of the samples with A360V, 35% were associated with M41L, 21% with D67N, 30% with K70R, 17% with L210W, 42% with T215Y/F, and 17% with K219Q/E

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