Drug resistance mutations in patients infected with HIV-2 living in Spain.
PMID: 21558334
2011
The Journal of antimicrobial chemotherapy
Abstract: No major mutations associated with drug resistance in HIV-1 were recognized in 29 PR, 20 RT and 5 INT sequences from antiretroviral-naive HIV-2 individuals, although natural polymorphisms with potential effects on susceptibility to PR inhibitors were recognized at 10 positions (L10V/I, V32I, M36I, M46I, I47V, Q58E, A71V/I, G73A, V82I and L89I/V) and for nucleoside reverse transcriptase inhibitors at three positions (T69N, V75I
HIV-1 drug resistance at antiretroviral treatment initiation in children previously exposed to single-dose nevirapine.
Result: Nineteen samples had major NRTI mutations, specifically K219E/Q (n=8), L74V (n=7), K70E (n=3), D67N (n=2) and L210W (n=1).
High prevalence of HIV-1 drug resistance among patients on first-line antiretroviral treatment in Lome, Togo.
PMID: 21663632
2011
Journal of the International AIDS Society
Result: Two patients had virus mutations indicative of the TAM-1 profile (M41L, L210W, T215S), and two of the TAM-2 profile (D67N, K70R, T215F, K219Q/R/E).
Table: K219E
Transmission of HIV drug resistance and non-B subtype distribution in the Spanish cohort of antiretroviral treatment naive HIV-infected individuals (CoRIS).
Abstract: The most prevalent resistance mutations were: T215 revertants (3.8%), D67NG (1.3%), K219QENR (1.2%) and M41L (1%), for NRTIs; K103N (3.2%), for NNRTIs; I54VLMSAT, M46I and L90M (0.7%), for PIs.
Moderate prevalence of transmitted drug resistance and high HIV-1 genetic diversity in patients from Mato Grosso State, Central Western Brazil.
Abstract: Drug resistance mutations were observed in 5.4%: nucleoside reverse transcriptase inhibitor mutations M41L (n = 1), D67N (n = 1), and K219E (n = 1), the non-nucleoside reverse transcriptase inhibitor mutation K103N (n = 1) and the protease inhibitor mutation L90M (n = 1).
Genotypic resistance at viral rebound among patients who received lopinavir/ritonavir-based or efavirenz-based first antiretroviral therapy in South Africa.
PMID: 21694608
2011
Journal of acquired immune deficiency syndromes (1999)
Result: One participant who received EFV+d4T+3TC had four RT mutations (A62V, K65R, M184V, and K219E) in addition to two NNRTI-associated mutations.
Transmitted drug resistance in the CFAR network of integrated clinical systems cohort: prevalence and effects on pre-therapy CD4 and viral load.
Discussion: In contrast, the clinical consequences of D67N/G and K219Q/E are not as well known.
Discussion: Our results give the first evidence that the transmission of D67N/G may have deleterious virological and immunological consequences in therapy-naive patients that may be compensated by K219Q/E.
Discussion: Similarly, we have observed several compensatory interactions among mutations that would otherwise mask the actual effects of individual mutations on CD4 or pVL (e.g., D67N/G and K219Q/E).
Discussion: The effects of D67N/G and K219Q/E on CD4 in our study were mirrored by significant effects on pVL; i.e., substitutions at D67 were causally associate
Drug resistance patterns and virus re-suppression among HIV-1 subtype C infected patients receiving non-nucleoside reverse transcriptase inhibitors in South Africa.
PMID: 21927716
2011
Journal of AIDS & clinical research
Discussion: Among eight patients with TAMs, the most common pathway (seen in 6/8 patients) was TAM-2 related (D67N, K70R, K219Q/R/E); and the rest (2/8) were mixed with the TAM-1 pathway (M41L, L210W, T215Y) extending similar prior Southern African observations.
A structural frame for understanding the role of thymidine analogue resistance mutations in resistance to zidovudine and other nucleoside analogues.
Introduction: With regard to subtype, in subjects infected with HIV-1 subtype B, the thymidine analogue mutations pathway 1 or TAM-1 (including mutations M41L, L210W and T215Y) is probably more frequent than the TAM-2 pathway (including mutations D67N, K70R, T215F and K219E/Q), although systematic studies of these pathways have not been done.
Method: RT mutations were identified from the International AIDS Society USA Drug (IAS-USA) mutation tables, spring 2008 (http://www.iasusa.org/resistance_mutations): M41L, K65R, D67N, insertion 69,
HIV mutation literature information.
PMID: 
2011
The Journal of antimicrobial chemotherapy
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