Abstract: Two pathways to loss of susceptibility to RO-0335 were observed, containing patterns of amino acid changes at either V106I/A plus F227C (with additional contributions from A98G, V108I, E138K, M230L and P236L) or V106I/Y188L (with a potential contribution from L100I, E138K and Y181C).
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: The complete list of etravirine RAMs was defined as V90I, A98G, L100I, K101E/H/P, V106I, E138A, V179D/F/T, Y181C/I/V, G190A/S and M230L.
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, K101E, PMID: 19320243
2009
Antiviral 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
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)
Method: Etravirine-resistance mutations were defined as mutations associated in the DUET studies with a decreased virological response to etravirine: V90I, A98G, L100I, K101E/H/P, V106I, E138A, V179D/F/T, Y181C/I/V, G190A/S, and M230L.
Method: The mutations V90I, A98G, V106I, E138A, and V179D/T were considered to be less important indicators of etravirine resistance because they are polymorphic (particularly PMID: 20190870
2009
HIV therapy
Introduction: The development of K65R and Q151M may be facilitated for HIV-2 variants originating from West Africa (Senegal and Portugal), harboring NNRTI mutations (K101A, V106I, V179I, Y181I, Y188L and G190A) and TAMs/NAMs (T69N, V75I, V118I, L210N, T215S and K219E) as natural polymorphisms.
Evolution of genetic diversity and drug resistance mutations in HIV-1 among untreated patients from Mali between 2005 and 2006.
PMID: 18556706
2008
The Journal of antimicrobial chemotherapy
Abstract: Resistance mutations found in RT and PR genes are in agreement with the highly active antiretroviral therapy regimen available in Mali, except for V90I, V106I and A98G mutations which are associated with etravirine resistance, but polymorphic in non-B subtypes.
Evaluating the role of etravirine in the second-line antiretroviral therapy after failing an initial non-nucleoside reverse transcriptase inhibitor-based regimen in a resource-limited setting.
Conclusion: Etravirine RAMs include V90I, A98G, L100I, K101E/H/P, V106I, E138A, V179D/F/T, Y181C/I/V, G190A/S and M230L.
Table: V106I
A novel nonnucleoside analogue that inhibits human immunodeficiency virus type 1 isolates resistant to current nonnucleoside reverse transcriptase inhibitors.
PMID: 17116677
2007
Antimicrobial agents and chemotherapy
Abstract: A virus containing the double mutation V106I-Y181C emerged after 4 months, causing a sixfold increase in resistance.
In vitro selection of mutations in human immunodeficiency virus type 1 reverse transcriptase that confer resistance to capravirine, a novel nonnucleoside reverse transcriptase inhibitor.
HIV mutation literature information.
PMID: 
2010
Antiviral research
Browser Board
Co-occurred Entities
Filtrator
ViMRT