literature

HIV mutation literature information.

Structural studies on molecular mechanisms of Nelfinavir resistance caused by non-active site mutation V77I in HIV-1 protease.

PMID: 26695135 2015 BMC bioinformatics

Abstract: V77I is known to cause Nelfinavir (NFV) resistance in the subtype B population of HIV-1 protease.

Abstract: In this study, we have studied the effect of the V77I mutation in HIV-PR along with the co-occurring mutations L33F and K20T through multi-nanosecond molecular dynamics simulations.

Abstract: RESULTS: Two HIV-PR mutants have been considered in this study - the Double Mutant Protease (DBM) V77I-L33F and Triple Mutant Protease (TPM) V77I-K20T-L33F.

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

PMID: 26543866 2015 BioMed research international

Result: With respect to accessory or secondary mutations, the most frequent were L63P (60.7%), M36I (41.1%), I93L (40.1%), I62V (39%), V77I (35.8%), A71V (24.9%), and L10I (24.7%) (Figure 1(d)).

MOLECULAR TRACING OF HETEROSEXUAL HIV-1 TRANSMISSION IN GEORGIA.

PMID: 26355316 2015 Georgian medical news

Abstract: Of these 16 events, viruses from 14 pairs had genetic distance less than 0.015.Mutation A62V was seen in samples from 5 pairs, of them samples from 4 pairs additionally had V77I mutation.

Effectiveness of a Treatment Switch to Nevirapine plus Tenofovir and Emtricitabine (or Lamivudine) in Adults with HIV-1 Suppressed Viremia.

PMID: 26107265 2015 PloS one

Table: V77I

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

PMID: 25962088 2015 PloS one

Result: Instead, T74S (2.5%) that is a common accessory mutation and V77I (2.5%) that confers moderate resistance to indinavir (IDV), nelfinavir (NFV) and saquinavir (SQV) were identified in our samples.

Table: V77I

Mutations in the reverse transcriptase and protease genes of human immunodeficiency virus-1 from antiretroviral naive and treated pediatric patients.

PMID: 25674767 2015 Viruses

Table: V77I

Phenotypic characterization of virological failure following lopinavir/ritonavir monotherapy using full-length Gag-protease genes.

PMID: 25096075 2014 The Journal of antimicrobial chemotherapy

Result: A number of protease polymorphisms were present both at baseline and time of treatment failure: N37S, P39Q, I62V, L63P, V77I and I93L.

Result: A number of polymorphisms were present in protease at both screening and failure: E35D, L63P, I72V, V77I and I93L (Table S1).

Characteristics of HIV-1 natural drug resistance-associated mutations in former paid blood donors in Henan Province, China.

PMID: 24586665 2014 PloS one

Abstract: Polymorphism mutation sites with mutation rates in the protease region higher than 60.0% were: L63A/P/S/T 89.7%, V77I 82.2%, I72E/M/K/T/V 80.4%, I93L 75.7%, and E35D 72.9%.

Result: The sites with mutation rates higher than 60.0% included: L63A/P/S/T 89.7% (96/107), among which L63P was 70.1% (75/107); V77I 82.2% (88/107); I72E/M/K/T/V 80.4% (86/107), among which I72V was 63.6% (75/107); I93L 75.7%; E35D 72.9%.

Natural polymorphisms and unusual mutations in HIV-1 protease with potential antiretroviral resistance: a bioinformatic analysis.

PMID: 24629078 2014 BMC bioinformatics

Conclusion: Furthermore, the presence of a high rate of L63P, I93L, V77I and I62V polymorphisms among the Mexican population is similar to that observed in patients that underwent antiretroviral treatments in other American and western European countries.

Result: According to the IAS-USA, the mutations associated with drug resistance, with a p >10%, were L10I, M36I, I62V, L63P, I64V, A71V/T, V77I, L90M, and I93L.

Persistence of frequently transmitted drug-resistant HIV-1 variants can be explained by high viral replication capacity.

PMID: 25575025 2014 Retrovirology

Table: V77I

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