Genetic diversity and antiretroviral resistance-associated mutation profile of treated and naive HIV-1 infected patients from the Northwest and Southwest regions of Cameroon.
Result: Eleven (25%, 11/44) of the RTRM were thymidine analogue mutations (T215FY [2.5%, 6/239], K70R [1.7%, 4/239] and 0.8% (2/239) each of D67N, L210W, M41L, and K219Q/E (Fig 2).
Table: K219E/Q
HIV Drug Resistance Mutations in Patients with HIV and HIV-TB Coinfection After Failure of First-Line Therapy: A Prevalence Study in a Resource-Limited Setting.
PMID: 31117863
2019
Journal of the International Association of Providers of AIDS Care
Table: K219Q
Human immunodeficiency virus type 1 drug resistance in a subset of mothers and their infants receiving antiretroviral treatment in Ouagadougou, Burkina Faso.
PMID: 30079168
2018
Journal of public health in Africa
Abstract: Other mutations such as T215F/Y, D67N/E, K70R, and K219Q were associated with intermediate resistance to TDF, AZT, and 3TC.
Result: Also, other DRM such as K70R (5.56%), K219Q (5.56%), T69D (5.56%), Y115F (5.56%) and K65R (5.56%) were detected with equal rates in mothers and were associated with resistance to (AZT, 3TC, TDF), 3TC, DDI, ABC and 3TC respectively.
Discussion: Others mutations detected such as T215F/Y, D67N/E, K70R, and K219Q are associated with intermediate resistance to TDF, AZT, and 3TC.
Distinct Pattern of Thymidine Analogue Mutations with K65R in Patients Failing Tenofovir-Based Antiretroviral Therapy.
PMID: 29084434
2018
AIDS research and human retroviruses
Introduction: Based on significant previous research of DRMs, TAMs have been described to associate into one of two distinct pathways: TAM-1 (M41L, L210W, T215Y) or TAM-2 (D67N, K70R, T215F, K219E/Q).
Introduction: In viruses lacking K65R, the TAMs observed included a broader array of primarily TAM-2, including K219E, D67N, K70R, T215F, and K219Q, and in one patient with TAM-1, T215Y.
Introduction: This was not true of other TAMs present in patients on 1L TDF, such as PMID: 29584723
2018
PLoS medicine
Result: The majority (92.6%) of all 27 low-frequency mutations identified in our study were detected in PBMCs, and many were consistent with APOBEC mutations (e.g., M184I and G73S) or regions of homopolymers, such as K101E and K219Q (Tables 2 and 3).
Table: K219Q
Impact of Antiretroviral Regimens on Cerebrospinal Fluid Viral Escape in a Prospective Multicohort Study of Antiretroviral Therapy-Experienced Human Immunodeficiency Virus-1-Infected Adults in the United States.
Result: Given the high frequency of M184V/I detected in all samples (28%, 56/197), these mutations were combined with thymidine-analog mutations (TAMs; ie, M41L, L210W, T215Y, D67N, K70R, T215F, K219Q/E) for analysis.
Risk factors and outcomes for the Q151M and T69 insertion HIV-1 resistance mutations in historic UK data.
Result: Study subject CY289, a Romanian citizen living in Cyprus, was infected with a sub-subtype F1 dual-class RT resistant strain carrying both K219Q and K103N mutations.
Antiretroviral resistance among HIV-1 patients on first-line therapy attending a comprehensive care clinic in Kenyatta National Hospital, Kenya: a retrospective analysis.
PMID: 30061964
2018
The Pan African medical journal
Abstract: Major NRTI mutations were detected in 11 patient samples, which included M184V (n = 6), M41L (n=3), D67N (n=2), K219Q (n=3) and T215F (n=2).
Result: Major NRTI mutations were detected in 11 patient samples, which included M184V (n=6), M41L (n=3), D67N (n=2), K219Q (n=3) and T215F (n=2).
Table: K219Q
The High Genetic Barrier of EFdA/MK-8591 Stems from Strong Interactions with the Active Site of Drug-Resistant HIV-1 Reverse Transcriptase.
Introduction: Moreover, we found that nine amino acid substitutions, namely, M41L, D67Delta, T69G, K70R, L74I, V75T, M184V, T215F, and K219Q (in HIV-1EFdAR), were associated with EFdA resistance.
Result: We previously selected an HIV-1EFdAR variant harboring M41L, D67Delta, T69G, K70R, L74I, V75T, M184V, T215F, and K219Q mutations (Figure 2A).
HIV mutation literature information.
PMID: 
2019
PloS one
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