literature

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: 23985909 2013 Journal of clinical microbiology

Abstract: All the wild-type and mutant alleles were unequivocally distinguished with plasmid templates, and the limits of detection were 1.56% for K219Q and K219E, 3.13% for L76V, 6.25% for K65R, K70R, L74V, L100I, K103N, K103R, Q151M, Y181C, and I47V, and 12.5% for M41L, K101P, K101E, V106A, V106M, Y115F, M184V,

PMID: 24009694 2013 PloS one

Table: K103R

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

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%).

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.

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

Comparison of predicted susceptibility between genotype and virtual phenotype HIV drug resistance interpretation systems among treatment-naive HIV-infected patients in Asia: TASER-M cohort analysis.

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.

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

Connection domain mutations in HIV-1 reverse transcriptase do not impact etravirine susceptibility and virologic responses to etravirine-containing regimens.

PMID: 21464253 2011 Antimicrobial agents and chemotherapy

Abstract: N348I or T369I was associated with reduced etravirine susceptibility when present with K101P or K103R/V179D.