Result: We also checked population sequences for additional AZT/3TC/NVP-selected resistance mutations like M41L, D67N, K70R, L210W, T215Y/F and K219QE for AZT, K65R for 3TC and L100I, K101P, V106A/M, V108I, Y188C/L/H and G190A for NVP.
HIV-1 phenotypic reverse transcriptase inhibitor drug resistance test interpretation is not dependent on the subtype of the virus backbone.
Introduction: This type of mutation consists of A98G, K101Q, V108I, and V179D/E.
Discussion: found the prevalence rate of H221Y in isolates from patients failing NVP treatment was 10.3% and the mutation was included in the top 10 and 15 determinants for NVP and EFV resistance, respectively, ranking even above some classical NNRTI resistance mutations, such as K101E, V108I, and G190E.
Clinical, virological and biochemical evidence supporting the association of HIV-1 reverse transcriptase polymorphism R284K and thymidine analogue resistance mutations M41L, L210W and T215Y in patients failing tenofovir/emtricitabine therapy.
Discussion: The preservation of NNRTI mutations in the viral genome of treated patients can be attributed to their small effect on viral fitness, as demonstrated for V108I, Y181C and G190A.
Identification of drug resistant mutations in HIV-1 CRF07_BC variants selected by nevirapine in vitro.
Discussion: For example, V108I has been reported to correlate with the
Discussion: Initial mutations A98G, V108I and Y181C appeared during the first 10 passages in the presence of 800 nM NVP (4-fold of EC50), while double mutations I135T/I382L were detected between passages 10 and 15 (Figure 4).
Discussion: Similarly, V108I has been found in both subtype B and C viruses, whereas A98S was only detected in subtype C virus.
Discussion: The low mutation barrier at these positions suggests that A98G, V108I and Y181C may be found in NVP treated patients infected with CRF07_BC with high possibility.
Monitoring HIV viral load in resource limited settings: still a matter of debate?
Result: The most frequent NNRTI mutations were K103N/S (27.8%), followed by Y181C (22.2%), V108I and G190A (16.7%), Y181V (11.1%), K101E and Y188L (5.6%) (Figure 2).
Table: V108I
Low prevalence of transmitted K65R and other tenofovir resistance mutations across different HIV-1 subtypes: implications for pre-exposure prophylaxis.
PMID: 23305651
2012
Journal of the International AIDS Society
Table: V108I
Differences in reversion of resistance mutations to wild-type under structured treatment interruption and related increase in replication capacity.
Method: The final list of mutations included M41L, E44D, D67N, T69D, K70R, L74V, L100I, K103N, V108I, V118I, Y181C, M184V, Result: Other mutations that were less frequent but associated with a large increase in RC included E44D, T69D, D67N, and 2 Non-Nucleoside RT inhibitors (NNRTI) mutations (namely V108I and Y181C).
Docking analysis and resistance evaluation of clinically relevant mutations associated with the HIV-1 non-nucleoside reverse transcriptase inhibitors nevirapine, efavirenz and etravirine.
Abstract: The most common indicator of treatment failure for efavirenz was K103N mutation present in 56.7% of the patients where the drug failed, followed by V108I, L100I, and G190A.
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,
ViMRT
HIV mutation literature information.
PMID: 
2012
PloS one
