literature

HIV mutation literature information.

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

Abstract: In treated patients, K20M, D30N, G73S, I84V, and L90M, were more prevalent in subtype B, and K20T and N88S were more prevalent in subtype F1.

Method: Mutations D30N (NFV), V32I (LPV), M46I/L (IDV/RTV), I47V/A (LPV/RTV), G48V (SQV), I50L/V (APV), V82A/F/T/S (LPV/IDV/RTV), I84V (APV/IDV/RTV) and L90M (SQV/NFV) were considered as major resistance mutations and were analyzed separately for each

Non-cleavage site gag mutations in amprenavir-resistant human immunodeficiency virus type 1 (HIV-1) predispose HIV-1 to rapid acquisition of amprenavir resistance but delay development of resistance to other protease inhibitors.

PMID: 19176623 2009 Journal of virology

Abstract: Recombinant HIV-1 clones containing NFV resistance-associated mutations, such as D30N and N88S, had increased susceptibilities to APV, suggesting that antiretroviral regimens including both APV and NFV may bring about favorable antiviral efficacy.

Proteochemometric modeling of drug resistance over the mutational space for multiple HIV protease variants and multiple protease inhibitors.

PMID: 19391634 2009 Journal of chemical information and modeling

Abstract: The model revealed the most deleterious mutations in the protease to be D30N, V32I, G48V, I50V, I54V, V82A, I84V, and L90M.

Clinical relevance of substitutions in the connection subdomain and RNase H domain of HIV-1 reverse transcriptase from a cohort of antiretroviral treatment-naive patients.

PMID: 19428602 2009 Antiviral research

Result: However, HIV-1 protease mutations D30N and M36I that are responsible for resistance to NFV and HIV-1 RT D67N mutation that is responsible for AZT resistance eventually emerged.

Role of atazanavir in the treatment of HIV infection.

PMID: 19436623 2009 Therapeutics and clinical risk management

Introduction: Mutations more significant to be included in the GIQ model are the following: L10F/I/V, K20M/R, L24I, D30N, V32I, L33F, M36I/L, I47V/A, G48V, I50V, I50L, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73S, V77I, V82A/F/T, I84V, N88D/S and

Differences in resistance mutations among HIV-1 non-subtype B infections: a systematic review of evidence (1996-2008).

PMID: 19566959 2009 Journal of the International AIDS Society

Abstract: The main differences are reflected in the discoveries that: (i) the non-nucleoside reverse transcriptase inhibitor resistance mutation, V106M, has been seen in subtype C and CRF01_AE, but not in subtype B, (ii) the protease inhibitor mutations L89I/V have been reported in C, F and G subtypes, but not in B, (iii) a nelfinavir selected non-D30N containing pathway predominated in CRF01_AE and CRF02_AG, while the emergence of D30N is favoured in subtypes B and D, (iv) studies on thymidine analog-treated subtype C infections from South Africa, Botswana and Malawi have reported a higher frequency of the K65R resistance mutation than that typically seen with subtype B.Additionally, some substitutions that seem to impact non-B viruses differentially a

HIV type-1 clade C resistance genotypes in treatment-naive patients and after first virological failure in a large community antiretroviral therapy programme.

PMID: 19578237 2009 Antiviral therapy

Discussion: Other mutations that are more likely to impact on the future use of a protease inhibitor, including D30N, M46I, I47V, I50V and V82A/F, were present, but in a minority of individuals, with only a single mutation noted per individual.

Human immunodeficiency virus type 1 protease-correlated cleavage site mutations enhance inhibitor resistance.

PMID: 19706699 2009 Journal of virology

Abstract: Several patterns were frequently observed, including mutations in the NC-p1 cleavage site in combination with I50L, V82A, and I84V within the protease and mutations within the p1-p6 cleavage site in combination with D30N, I50V, and I84V within the protease.

Five-year follow up of genotypic resistance patterns in HIV-1 subtype C infected patients in Botswana after failure of thymidine analogue-based regimens.

PMID: 19852859 2009 Journal of the International AIDS Society

Abstract: The most frequent PI mutations involving resistance to NFV were L90M (25.2%) and D30N (16.2%), but mutations at positions K45Q and D30N were often observed in tandem (P = 60.5, J = 50; p = 0.002; Group 2) alongside Q61E in 42.8% of patients who received ZDV/3TC.

Effects of HIV type-1 immune selection on susceptability to integrase inhibitor resistance.

PMID: 19918099 2009 Antiviral therapy

Discussion: Specific subtype drug resistance interactions have been described in other drug contexts, such as the more rapid selection of RT K65R on tenofovir in subtype C viruses and the low prevalence of nelfinavir-associated D30N in subtype C viruses, among others.

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