Low frequency nonnucleoside reverse-transcriptase inhibitor-resistant variants contribute to failure of efavirenz-containing regimens in treatment- experienced patients.
PMID: 20102272
2010
The Journal of infectious diseases
Table: V106M
Viremia and drug resistance among HIV-1 patients on antiretroviral treatment: a cross-sectional study in Soweto, South Africa.
Abstract: M184V/I, K103N and V106A/M were the most common mutations.
Discussion: Thus, M184V/I, K103N and V106A/M were the most common mutations due to lamivudine and NNRTI use.
Constrained patterns of covariation and clustering of HIV-1 non-nucleoside reverse transcriptase inhibitor resistance mutations.
PMID: 20462946
2010
The Journal of antimicrobial chemotherapy
Method: We performed multidimensional scaling on the pairwise association data using a matrix D of dissimilarity coefficients (JD = 1 - J, where J is the Jaccard similarity coefficient) for the 22 mutations found in the significantly positively associated pairs (corrected P < 0.05): A98G, L100I
Table: V106M
Discussion: For example, nevirapine selects for V106A, Y181C/I/V and G190A significantly more frequently than efavirenz, whereas efavirenz preferentially selects for L100I, K101P, V106M, Y188L, G190S and P225H.
Nucleic acid template and the risk of a PCR-Induced HIV-1 drug resistance mutation.
Discussion: For example, subtype C viruses are significantly more likely than subtype B viruses to develop the non-nucleoside RT-inhibitor-resistance mutation V106M because this mutation requires a single substitution for subtype C viruses (GTG ATG) but two substitutions for subtype B viruses (GTA ATG ).
Distinct mutation pathways of non-subtype B HIV-1 during in vitro resistance selection with nonnucleoside reverse transcriptase inhibitors.
PMID: 20805392
2010
Antimicrobial agents and chemotherapy
Abstract: With efavirenz (EFV), F227C and V106M were the major mutations responsible for viral breakthrough in subtype A viruses, whereas a single pathway (G190A/V106M) accounted for mutation development in subtype C viruses.
Nevirapine resistance and breast-milk HIV transmission: effects of single and extended-dose nevirapine prophylaxis in subtype C HIV-infected infants.
Method: NVP-R was defined by mutations present at the following amino acid sites: L100I, K101E/P, K103N/S, V106A/M, V108I, Y181C/I/V, Y188C/L/H, or G190A/S/E based on recommendations from International AIDS Society-USA Drug Resistance Mutations and Stanford University drug-resistance database.
Table: V106A/M
Table: V106M
Persistent minority K103N mutations among women exposed to single-dose nevirapine and virologic response to nonnucleoside reverse-transcriptase inhibitor-based therapy.
Abstract: These included V90I, A98G, L100I, K1O1E/P/Q, K103H/N/S/T, V106A/I/M, V108I, E138G/K/Q, V179D/E/F/G/I, Y181C/I/V, Y188C/H/L, V189I, G190A/C/E/Q/S, H221Y, P225H, F227C/L, M230I/L, P236L, K238N/T and Y318F
The public health approach to identify antiretroviral therapy failure: high-level nucleoside reverse transcriptase inhibitor resistance among Malawians failing first-line antiretroviral therapy.
Method: NNRTI mutations included K103N, Y181C, Y181I, G190A, G190S, V108I, Y188L, V106M, P225H, and K103NS.
Result: The most frequent NNRTI mutations were Y181C (55%), G190A (30%), K103N (28%), K101E (15%), Y188L (8%), V106M (7%), Y181I (6%), K103N/S (2%), PMID: 19552593
2009
AIDS research and human retroviruses
Introduction: Eight infants had mutations detected by ViroSeq [Y181C (n = 4), K103N (n = 1), V106M (n = 1), Y188C (n = 1), and V179D+K103R (n = 1)], and four infants had resistance detected by LigAmp only (all with Y181C, at 1.2%, 1.4%, 3.5%, and 7.8%; one infant also had G190A at 1.9%).
Introduction: Thirty-six (45.0%) of the 80 infants had at least one NVP resistance mutation detected; the mutations identified were Y181C (n = 28), K103N (n = 9), Y188C (n = 3), G190A (n = 30),
HIV mutation literature information.
PMID: 
2010
The Journal of infectious diseases
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