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 HIV mutation literature information.


  HIV-1 Resistance Dynamics in Patients With Virologic Failure to Dolutegravir Maintenance Monotherapy.
 PMID: 29617822       2018       The Journal of infectious diseases
Abstract: INSTI-RAMs (S230R, R263K, N155H, and E92Q+N155H) were detected in 4 patients, no INSTI-RAMs were detected in 4 patients, and sequencing of the integrase gene was unsuccessful in 2 patients.


  Selective resistance profiles emerging in patient-derived clinical isolates with cabotegravir, bictegravir, dolutegravir, and elvitegravir.
 PMID: 30119633       2018       Retrovirology
Table: S230R


  Occurrence of the S230R integrase strand inhibitor mutation in a treatment-naive individual case report.
 PMID: 29617824       2018       The Journal of infectious diseases
Abstract: Conclusions: Our data indicate that the S230R substitution is comparable to the previously reported R263K substitution in some respects.
Abstract: Methods: We evaluated the effect of the S230R substitution in regard to integrase enzyme activity, viral infectivity, replicative capacity, and susceptibility to different INSTIs by biochemical and cell-based assays.
Abstract: Our study aims to explain the underlying mechanism related to the emergence of a S230R substitution in patients who experienced virologic failure while using DTG monotherapy.


  Resistance to HIV Integrase Inhibitors: About R263K and E157Q Mutations.
 PMID: 29346270       2018       Viruses
Introduction: In this latter, VF occurred at week 120 with a viral load of 622 c/mL and R263K was detected added to A49G and S230R integrase mutations.


  Molecular evolution of HIV-1 integrase during the 20 years prior to the first approval of integrase inhibitors.
 PMID: 29137637       2017       Virology journal
Method: 26, September 2016), HIV-GRADE (http://www.hiv-grade.de, version January 16, 2017), and Rega (https://rega.kuleuven.be/cev/avd/software/rega-algorithm, v9.0.1, October 29, 2013) were considered: A49G, H51Y, V54I, L68IV, L74I, E92V, Q95K, H114Y, G118R, S119R, T124A, A128T, E138T, G140C, Y143AGS, P145S, Q146IKLPR, Q148EG,  PMID: 28637235       2017       The Journal of antimicrobial chemotherapy
Abstract: The virus from this mouse had mutations E138K, G140S, Q148H, N155H and S230R, was highly resistant to both raltegravir (EC50 of >1000 nM) and dolutegravir (EC50 of 550 nM), and replicated to levels similar to those of control viruses in PBMCs.


  HIV-1 strains belonging to large phylogenetic clusters show accelerated escape from integrase inhibitors in cell culture compared with viral isolates from singleton/small clusters.
 PMID: 28472323       2017       The Journal of antimicrobial chemotherapy
Result: The infrequent appearance of S230R, E157Q, G163R or G59E minority species (<10%) occurred in some large cluster selections at selected weeks of passage but failed to accumulate over time.
Result: The presence of secondary (accessory) mutations, including T66I, E157Q, G163R and S230R, can increase levels of resistance and/or viral fitness (Figures4b and).
Result: The second isolate, belonging to cluster 185 (14637), developed resistance with viruses coexpressing N155H (99.5%), Q95K (97.5%) and S230R (99.6%) as the dominant quasi-species (Figure6b).


  Prevalence of Integrase Strand Transfer Inhibitors (INSTI) Resistance Mutations in Taiwan.
 PMID: 27779200       2016       Scientific reports
Method: Besides these three major mutations, the integrase substitutions with a Stanford HIVdb score 10 to at least one INSTI were included, such as H51Y,
Result: In INSTI-naive patients, the resistance mutations included L74M (n = 28), E92V (1), Q95K (4), T97A (4), E138AK (3), Y143S (1), V151AL (1), N155S (9), E157Q (11), G163K/R (5), S230R (1) and R263K (4) (Supplementary Table 3).


  Lack of integrase inhibitors associated resistance mutations among HIV-1C isolates.
 PMID: 26626277       2015       Journal of translational medicine
Discussion: This includes T66IAK, E92Q, F121Y, G140SA, Y143HCR, Q146P, S147G, Q148KHR, and N155HS; (2) minor INI-resistance mutations were defined as non-polymorphic or minimally polymorphic mutations that reduce INI susceptibility H51Y, L74 M, T97A, E138AK, S153Y,


  Resistance against Integrase Strand Transfer Inhibitors and Relevance to HIV Persistence.
 PMID: 26198244       2015       Viruses
Introduction: Resistance mutations that were found in viral isolates from treatment-naive participants who experienced treatment failure during the initial dose-ranging Protocol 004 clinical trial were: L74L/M, V151I, N155H, Y143R and S230R in integrase (IN) and M184M/I/V and K65K/R in RT (Table 1).



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