literature

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: These mutations included: (i) 46 non-polymorphic NNRTI-selected mutations at 28 positions (I94L, A98G, L100I, K101E/H/N/P, K102N, K103H/N/S/T,

PMID: 20836706 2010 AIDS research and human retroviruses

Abstract: Mutations included E138A (etravirine resistance associated) and L210LS (thymidine analog mutation).

Antiretroviral drug susceptibility among drug-naive adults with recent HIV infection in Rakai, Uganda.

PMID: 19276794 2009 AIDS (London, England)

Result: Seven of the 104 samples (6.7%) had a mutation associated with NRTI resistance (one mutation in each sample: M41L (n = 2), E44D (n = 3), V118V/I (n = 1), K219K/R (n = 1)), and one sample had a mutation associated with NNRTI resistance (E138A).

Emergence of primary NNRTI resistance mutations without antiretroviral selective pressure in a HAART-treated child.

PMID: 19277127 2009 PloS one

Result: Among P50 sequences the mutations A98S, K101E, I135T and E138A were observed in all isolates.

Result: M50 sequences also showed mutations A98S, I135T and E138A.

Additional HIV-1 mutation patterns associated with reduced phenotypic susceptibility to etravirine in clinical samples.

PMID: 19474648 2009 AIDS (London, England)

Abstract: Etravirine phenotypic fold changes were 380-1400 for K101P + E138A/G/Q + K103N/S/T + V179I and 12-130 for K101P + (K103S +/- V179I) in the absence of E138A/G/Q.

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: 18687142 2008 Retrovirology

Result: Among mutations selected by raltegravir or elvitegravir that have not been shown to directly reduce susceptibility, L74R, Q95K, E138A/K, and H183P were conserved, whereas V54I, L68V, L74M, T97A, V151I,

Discussion: Most accessory INI-resistance mutations including L74R, Q95K, E138A/K, H183P, Y226C/D/F/H, S230R, and D232N were also nonpolymorphic.

Etravirine: a second-generation NNRTI for treatment-experienced adults with resistant HIV-1 infection.

PMID: 19881888 2008 Future HIV therapy

Conclusion: Etravirine RAMs include V90I, A98G, L100I, K101E/H/P, V106I, E138A, V179D/F/T, Y181C/I/V, G190A/S and M230L.

Introduction: More recently, further statistical analysis of the pooled 24-week DUET data expanded the original list of 13 etravirine RAMs to 17 with the addition of K101H, E138A, V179T and M23L (Table 5).

Table: E138A

Site-directed mutagenesis of human immunodeficiency virus type 1 reverse transcriptase at amino acid position 138.

PMID: 11162823 2001 Virology

Abstract: The Glu138Lys RT mutant virus had the most marked resistance to TSAOs, followed by the Glu138Gln, Glu138Phe, Glu138Gly, Glu138Tyr, and Glu138Ala virus mutants.

Abstract: The mutant Glu138Asp, Glu138Lys, Glu138Gln, Glu138Ala, and Glu138Gly RTs retained marked catalytic activity.

"Presence of 2',5'-Bis-O-(tert-butyldimethylsilyl)-3'-spiro-5""-(4""-amino-1"",2""-oxath iole-2"",2""-dioxide) (TSAO)-resistant virus strains in TSAO-inexperienced HIV patients."

PMID: 10875608 2000 AIDS research and human retroviruses

Abstract: E138K, not E138A, is a known TSAO-specific resistance mutation, emerging under selective pressure in vitro.

Abstract: As TSAO derivatives have not been used in the clinical setting, the presence of the E138A mutation at a frequency of 6.7% in our study of 90 TSAO-inexperienced HIV-seropositive individuals implies that 138A of the RT must be a natural variant and that the mutant virus is replication competent.

Abstract: HIV-1 samples from six patients undergoing diverse anti-HIV therapies possessed the E138A mutation in their reverse transcriptase (RT) genome.