HIV mutation literature information.


  Virological failure rates and HIV-1 drug resistance patterns in patients on first-line antiretroviral treatment in semirural and rural Gabon.
 PMID: 23199801       2012       Journal of the International AIDS Society
Result: Five additional viruses were predicted to be possibly resistant to ETV, including three viruses harbouring the E138A/G/Q/R DRM, one with the three DRMs K101E/H/I/P/R, Y181C, and G190A/S, and one with the three DRMs V90I, K101E/H/I/P/R, and G190A/S.
Result: Major NNRTIs DRMs were also obtained at positions P225H (n=12), K101E (n=11), Y181C (n=10), G190A (n=7), Y188L (n=6), V90I (n=5),  PMID: 22818969       2012       Journal of clinical virology
Abstract: Four samples (15%) had a major rilpivirine resistant mutation (E138G, K101E and E138A), 3 of which were detected by UDPS.
Abstract: The 11 RAMs not detected by bulk sequencing were A98G (n=2), L100I (n=3), K101E (n=2), V106I (n=3) and E138G (n=1).


  Effect of mutations at position E138 in HIV-1 reverse transcriptase on phenotypic susceptibility and virologic response to etravirine.
 PMID: 21637112       2011       Journal of acquired immune deficiency syndromes (1999)
Abstract: E138G, K, and Q were added to the existing etravirine-weighted genotypic score including 17 etravirine resistance-associated mutations.
Abstract: Site-directed mutants harboring E138A/G/K/Q/R or S showed etravirine fold change values of 2.9, 2.4, 2.6, 3.0, 3.6, and 2.8, respectively.


  HIV-1 drug resistance at antiretroviral treatment initiation in children previously exposed to single-dose nevirapine.
 PMID: 21633285       2011       AIDS (London, England)
Result: NNRTI minor mutations were also detected, specifically E138A (n=20), V179D (n=7), V90I (n=3) and A98G (n=1), as well as the NNRTI-associated polymorphisms K101Q/T (n=3), E138G/S (n=3), V179A (n=2), H221Y (n=2) and L234P (n=1).


  Update of the drug resistance mutations in HIV-1: December 2010.
 PMID: 21245516       2010       Topics in HIV medicine
Abstract: This update includes 9 new mutations- E138G and E138K for etravirine (Haddad M et al, CROI, 2010; Abstract 574, and Vingerhoets J et al, Antivir Ther, 2010;15 [Suppl 2]:A125); E92Q for raltegravir (Geretti AM et al, Antivir Ther, 2010;15 [Suppl 2]:A62; Cooper et al, N Engl J Med, 2008;359:355-365; and Malet I et al, Antimicrob Agents Chemother, 2008;52:1351-1358); and M36L, M36V, H69R, L89I, L89M, and L89V for tipranavir/ritonavir.


  TMC278, a next-generation nonnucleoside reverse transcriptase inhibitor (NNRTI), active against wild-type and NNRTI-resistant HIV-1.
 PMID: 19933797       2010       Antimicrobial agents and chemotherapy
Abstract: NNRTI RAMs emerging in HIV-1 under selective pressure from TMC278 included combinations of V90I, L100I, K101E, V106A/I, V108I, E138G/K/Q/R, V179F/I, Y181C/I, V189I, G190E, H221Y, F227C, and M230I/L.


  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.


  Compilation and prevalence of mutations associated with resistance to non-nucleoside reverse transcriptase inhibitors.
 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


  Site-directed mutagenesis of human immunodeficiency virus type 1 reverse transcriptase at amino acid position 138.
 PMID: 11162823       2001       Virology
Abstract: Mixtures of Glu138Lys RT mutant virus with the other virus clones mutated at the 138 position resulted in all cases, except for the Glu138Asp and Glu138Gly RT mutant viruses, in an outgrowth of the Glu138Lys RT mutant virus.
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,



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