HIV mutation literature information.


  The impact of HIV-1 reverse transcriptase polymorphisms on responses to first-line nonnucleoside reverse transcriptase inhibitor-based therapy in HIV-1-infected adults.
 PMID: 24157905       2013       AIDS (London, England)
Abstract: Polymorphisms associated with virologic failure occurred at codons 90 (mostly V90I), 98 (mostly A98S), and 103 (mostly K103R), with adjusted hazard ratios of 1.78 (1.15-2.73; P = 0.009), 1.55 (1.16-2.08; P = 0.003), and 1.75 (1.00-3.05: P = 0.049), respectively.


  Increased risk of Q151M and K65R mutations in patients failing stavudine-containing first-line antiretroviral therapy in Cambodia.
 PMID: 24015311       2013       PloS one
Result: The most frequently detected mutations were: M184I/V (92.3%), Y181C/I/V (47.1%), T215I/C/F/N/S (38.8%), D67E/G/N (37.3%), K103N/R/S (33.9%), and G190A/Q/S (32.5%).


  Potential elucidation of a novel CTL epitope in HIV-1 protease by the protease inhibitor resistance mutation L90M.
 PMID: 24015196       2013       PloS one
Result: The mutations RT:K102R and RT:K103R associated with HLA:B*48 mutation also occur at higher frequencies in the PR:90L set.
Table: K103R


  Prevalence and mutation patterns of HIV drug resistance from 2010 to 2011 among ART-failure individuals in the Yunnan Province, China.
 PMID: 24009694       2013       PloS one
Table: K103R


  Transmission patterns of HIV-subtypes A/AE versus B: inferring risk-behavior trends and treatment-efficacy limitations from viral genotypic data obtained prior to and during antiretroviral therapy.
 PMID: 23469241       2013       PloS one
Result: The latter differed significantly in the frequencies of the major resistance RT mutations T215FY and K219QE (NRTI) and of several secondary/accessory mutations, including: the protease mutations I13V, M36I, I62V, L63P, A71V, V77I, L89M and I93L (Table 6) and the RT mutations A98S, K101N, K103R and V179I (Table 5).
Table:  PMID: 23095645       2012       BMC research notes
Discussion: V179D also confers significant resistance to NNRTIs when presented together with K103R .
Discussion: Only 2 patients had a combination of K103R and V179D.


  Zidovudine (AZT) monotherapy selects for the A360V mutation in the connection domain of HIV-1 reverse transcriptase.
 PMID: 22363673       2012       PloS one
Table: K103K/R


  Biochemical, inhibition and inhibitor resistance studies of xenotropic murine leukemia virus-related virus reverse transcriptase.
 PMID: 21908397       2012       Nucleic acids research
Abstract: We demonstrated that XMRV RT mutants K103R and Q190M, which are equivalent to HIV-1 mutants that are resistant to tenofovir (K65R) and AZT (Q151M), are also resistant to the respective drugs, suggesting that XMRV can acquire resistance to these compounds through the decreased incorporation mechanism reported in HIV-1.
Method: Drug resistant XMRV RT mutants Q190M and K103R (equivalent to HIV-1 Q151M RT and K65R) were generated by site-directed mutagenesis using forward and reverse primers 2 and 3.
Result: Similarly, the K103R XMRV RT mutant enzyme was less


  'Sentinel' mutations in standard population sequencing can predict the presence of HIV-1 reverse transcriptase major mutations detectable only by ultra-deep pyrosequencing.
 PMID: 21890537       2011       The Journal of antimicrobial chemotherapy
Abstract: METHODS: We focused our attention on three reverse transcriptase (RT) mutations (T69S, L210M and K103R) easily detected by standard population sequencing [i.e.
Abstract: Moreover, the presence of L210M or T69S viruses by GRT significantly correlated with that of minority thymidine analogue mutations by UDPS (6/20 patients carrying HIV-1 strains with T69S/L210M versus 0/20 patients carrying HIV-1 having K103R or none of these mutations; P = 0.03).
Abstract: No association was found for K103R by GRT.


  HIV-1 drug resistance at antiretroviral treatment initiation in children previously exposed to single-dose nevirapine.
 PMID: 21633285       2011       AIDS (London, England)
Result: Similar to K103R, this polymorphism falls out of the primer binding region and thus the low positive AS-PCR value was assumed to reflect the presence of K103N.
Result: The polymorphism K103R was detected by population sequencing in 4 samples, and did not appear to affect the assay in that all 4 samples were negative by AS-PCR.
Discussion: However, in some cases polymorphisms can be tolerated as evidenced by the K103R genotype which did not interfere with the K103N assay.



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