literature

HIV mutation literature information.

Revealing the binding and drug resistance mechanism of amprenavir, indinavir, ritonavir, and nelfinavir complexed with HIV-1 protease due to double mutations G48T/L89M by molecular dynamics simulations and free energy analyses.

PMID: 25513833 2015 Biochemistry

Abstract: A 1.9 A resolution crystal structure was solved for PRG48T/L89M bound with saquinavir (PRG48T/L89M-SQV) and compared to the crystal structure of PRWT bound with saquinavir (PRWT-SQV).

Abstract: HIV drug resistance continues to emerge; consequently, there is an urgent need to develop next generation antiretroviral therapeutics.1 Here we report on the structural and kinetic effects of an HIV protease drug resistant variant with the double mutations Gly48Thr and Leu89Met (PRG48T/L89M), without the stabilizing mutations Gln7Lys, Leu33Ile, and Leu63Ile.

Abstract: Kin

Characterization of HIV drug resistance mutations among patients failing first-line antiretroviral therapy from a tertiary referral center in Lusaka, Zambia.

PMID: 25754408 2015 Journal of medical virology

Discussion: A prior study of antiretroviral drug-nave HIV-1-infected Zambian adults (n=28) demonstrated a high frequency of pre-existing minor mutations in the protease gene:including I93L (92%), L89M (79%), and M36I (79%):which corroborates results from our current study (Handema et al., 2003).

Transmitted Drug Resistance Mutations in Antiretroviral-Naive Injection Drug Users with Chronic HIV-1 Infection in Iran.

PMID: 25962088 2015 PloS one

Result: We found no SDRMs to protease inhibitors (PIs); however, based on the mutations listed in the International Antiviral Society-USA (IAS-USA) panel, 13minor mutations were detected in the PR region, of which M36I, H69K, and L89M/V/I were found in all 40 (100%) andK20R/T was detected in 37 (92.5%) samples.

Table: L89M/V

Discussion: Moreover, in agreement with previous reports we identified high frequencies of M36I, H69K, L89M/V/I and K20R/T mutations that may be considered as polymorphic signatures within the protease region of CRF35_AD

Low Incidence of HIV-1C Acquired Drug Resistance 10 Years after Roll-Out of Antiretroviral Therapy in Ethiopia: A Prospective Cohort Study.

PMID: 26512902 2015 PloS one

Result: However, in all the 8 patients, naturally occurring minor mutations/polymorphic changes at PR region (positions M36I, R41K, H69K, L89M, and I93L) were observed.

The Evolving Genotypic Profile of HIV-1 Mutations Related to Antiretroviral Treatment in the North Region of Brazil.

PMID: 26543866 2015 BioMed research international

Discussion: L63P and A71T were associated with subtype B, whereas L10V, K20R, M36I, F53L, and L89M were linked to non-B subtypes.

HIV-1 subtype characteristics of infected persons living in southwestern Greece.

PMID: 26715861 2015 HIV/AIDS (Auckland, N.Z.)

Abstract: Protease substitutions I13V, E35D, M36I, R57K, H69K, and L89M, which serve as drug-resistance support mutations in subtype B, were present in the majority of subtype-A1 sequences of the population.

Result: Specifically, the E35D and M36I substitutions were present in 100% of cases, followed by substitutions H69K (99%), I13V (96%), L89M (95%), and R57K (93%), indicating that these sequence alterations may occur as genetic signatures in subtype A1.

Result: This involved six protease amino acid su

Zero prevalence of primary drug resistance-associated mutations to protease inhibitors in HIV-1 drug-naive patients in and around Aligarh, India.

PMID: 24423716 2014 Journal of infection in developing countries

Abstract: The most frequent mutations were H69K and I93L (52 of 52 strains), followed by I15V (80.7%), L19I (69.2%), M36I (67.3%), R41K (94.2%), L63P (61.5%), and L89M (82.7%).

Virological efficacy and immunological recovery among Ethiopian HIV-1 infected adults and children.

PMID: 24422906 2014 BMC infectious diseases

Result: In 3 patients, naturally occurring polymorphisms that may or may not have an impact on levels of drug resistance were found (mutations M36I, H69K and L89M) (Table 2).

HIV-1 diversity, transmission dynamics and primary drug resistance in Angola.

PMID: 25479241 2014 PloS one

Result: Similar findings were obtained for K14R, E35D and R57K in subtype A and for L89M in subtype G.

Structures of darunavir-resistant HIV-1 protease mutant reveal atypical binding of darunavir to wide open flaps.

PMID: 24738918 2014 ACS chemical biology

Method: The PRP51 construct contains 14 mutations (L10I, I15V, K20R, L24I, V32I, L33F, M36I, M46L, I54M, L63P, K70Q, V82I, I84V, and L89M) plus three other mutations Q7K to minimize autoproteolysis and C67A and C95A to prevent cysteine-induced aggregation.

Result: <

Result: Mutation L89M has not been analyzed previously in structures.

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