Abstract: All nine recombinant VSVG/HIV-mut pseudovirions (VSVG/HIV-wt, VSVG/HIV(-K103N), VSVG/HIV(-Y181C), VSVG/HIV(-L100I,K103N), VSVG/HIV(-Y188L), VSVG/HIV(-K103N,Y181C), VSVG/HIV(-K103N,P225H), VSVG/HIV(-K103N,Y188L), VSVG/HIV(-K103N,G109A) and VSVG/HIV(-K103N,V108I)) had high efficient infectivity.
Virological efficacy and emergence of drug resistance in adults on antiretroviral treatment in rural Tanzania.
Clinical and genotypic findings in HIV-infected patients with the K65R mutation failing first-line antiretroviral therapy in Nigeria.
PMID: 19644383
2009
Journal of acquired immune deficiency syndromes (1999)
Result: The most common NNRTI mutations included: Y181C (168, 49.7%), K103N (123, 36.4%), G190A (89, 26.3%), A98G (66, 19.5%), K101E (59, 17.5%), V108I (52, 15.4%), and V90I (41, 12.1%).
Minority variants associated with transmitted and acquired HIV-1 nonnucleoside reverse transcriptase inhibitor resistance: implications for the use of second-generation nonnucleoside reverse transcriptase inhibitors.
PMID: 19734799
2009
Journal of acquired immune deficiency syndromes (1999)
Result: Ten of the 12 samples had a total of 14 non-etravirine resistance mutations including V108I (n=6), P225H (n=3), K101N (n=1), Y188C (n=1).
Result: The accessory NNRTI-resistance mutations P225H (n=3), V108I (n=1), A98G (n=1), and H221Y (n=1) were detected in six of the samples.
Viremia, resuppression, and time to resistance in human immunodeficiency virus (HIV) subtype C during first-line antiretroviral therapy in South Africa.
Molecular characterization of human immunodeficiency virus type 1 (HIV-1) and HIV-2 in Yaounde, Cameroon: evidence of major drug resistance mutations in newly diagnosed patients infected with subtypes other than subtype B.
PMID: 17855574
2008
Journal of clinical microbiology
Abstract: Single mutations associated with resistance to nucleoside reverse transcriptase inhibitors (T215Y/F [n = 3]) and nonnucleoside reverse transcriptase inhibitors (V108I [n = 1], L100I [n = 1], and Y181C [n = 2]) were observed in 7 of 75 (9.3%) group M samples.
Structural basis for drug resistance mechanisms for non-nucleoside inhibitors of HIV reverse transcriptase.
Abstract: We found that the mutations K101A, P225H, Y318F and Y318W decreased RT heterodimer stability whereas K103N, V108I, V108W, Y181C, Y188L, G190A, G190E, G190W and P225W increased RT heterodimer stability.
Transmission networks of drug resistance acquired in primary/early stage HIV infection.
Abstract: A single amino acid substitution confers only moderate resistance to YM-215389; indeed, four amino acid substitutions (V106L, V108I, E138K and L214F) were necessary for high-level resistance.