Abstract: Two had SDRMs to nucleoside reverse-transcriptase inhibitors (D67G and L210W), three had SDRMs to nonnucleoside reverse transcriptase inhibitors (G190A, G190S, and K101E), and one had SDRMs to protease inhibitors (N88D).
Predicted susceptibility of etravirine in HIV patients experiencing virological failure secondary to non-nucleoside reverse transcriptase inhibitor resistance in Argentina.
PMID: 21592625
2011
Enfermedades infecciosas y microbiologia clinica
Abstract: ETR-RAMs were defined as V90I, A98G, L100I, K101E/H/P, V106I, E138A, V179D/F/T, Y181C/I/V, G190A/S, and M230L, and were analyzed according to the weighted mutation score to predict susceptibility (Vingerhoets 2008).
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
Table: G190S
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: K103N was the most commonly detected in 9 (25%) participants, V106M in 6 (16.7%), and G190S/A +/- Y188C/L in 6 (16.7%).
Nonnucleoside reverse transcriptase inhibitor-resistant HIV is stimulated by efavirenz during early stages of infection.
Abstract: Reverse transcriptase (RT) genotypes with the NNRTI resistance mutations K101E+G190S are highly resistant to efavirenz (EFV) and can develop during failure of EFV-containing regimens in patients.
Abstract: Additionally, we showed that another NNRTI, nevirapine (NVP), stimulated K101E+G190S virus replication during the early steps of infection similar to EFV, but that the newest NNRTI, etravirine (ETR), did not.
Abstract: We determined that EFV stimulates K101E+G190S virus during early infection and does not affect late steps of virus replication, such as increasing the amount of
Resistance patterns selected by nevirapine vs. efavirenz in HIV-infected patients failing first-line antiretroviral treatment: a bayesian analysis.
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, K70R/E, L74I/V, L100I, K103N, V106A/M, V108I, Q151M, Y181I/C, M184V, Y188C/L, G190A/S, L210W, T215Y/F, PMID: 22160938
2011
Virologica Sinica
Abstract: Genotypic drug resistance analysis showed significant increases in percentages of patients carrying HIV-1 strains with M41L, T215Y/F, D67N, K103N, G190A/S, Y181C/F or L210W mutations.
Antiretroviral drug resistance in HIV-infected patients in Colombia.
PMID: 19665910
2010
International journal of infectious diseases
Abstract: The most common mutations were 184V (n=48; 62.3%), 103N (n=37; 48.1%), G190A/S (n=9; 11.7%), and L90M (n=9; 11.7%).
N348I in HIV-1 reverse transcriptase decreases susceptibility to tenofovir and etravirine in combination with other resistance mutations.
Introduction: Since the presence of three or more NNRTI mutations V90I, A98G, L100I, K101E/P, V106I, V179D/F, Y181C/I/V and G190A/S results in no response to etravirine treatment, the presence of two of these NNRTI mutations and N348I at baseline may also reduce etravirine efficacy in vivo.
Pre-existing minority drug-resistant HIV-1 variants, adherence, and risk of antiretroviral treatment failure.
PMID: 20102271
2010
The Journal of infectious diseases
Discussion: Alternatively, the low-level EFV resistance conferred by Y181C could have allowed ongoing virus replication that led, in turn, to the later accumulation of other NNRTI resistance mutations such as K103N or G190S.
HIV mutation literature information.
PMID: 
2011
AIDS (London, England)
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