HIV mutation literature information.


  Selection of mutations in the connection and RNase H domains of human immunodeficiency virus type 1 reverse transcriptase that increase resistance to 3'-azido-3'-dideoxythymidine.
 PMID: 17507476       2007       Journal of virology
Abstract: Because it is not known whether AZT selects for mutations outside of the polymerase domain of RT, we carried out in vitro experiments in which HIV-1(LAI) or AZT-resistant HIV-1(LAI) (M41L/L210W/T215Y) was passaged in MT-2 cells in increasing concentrations of AZT.
Abstract: Mutations in the connection and RNase H domains were not selected starting with AZT-resistant virus (M41L/L210W/T215Y).
Abstract: The roles of A371V and Q509L in AZT resistance were confirmed by site-directed mutagenesis: A371V and Q509L together increased AZT resistance approximately


  Anti-retroviral drug resistance-associated mutations among non-subtype B HIV-1-infected Kenyan children with treatment failure.
 PMID: 17516531       2007       Journal of medical virology
Abstract: In 7 of 12 children, M184V appeared with one thymidine-analogue-associated mutation (TAM) as the first mutation, while the remaining 5 children had only TAMs appearing either individually (n = 2), or as TAMs 1 (M41L, L210W, and T215Y) and 2 (D67N, K70R, and K219Q/E/R) appearing together (n = 3).


  Molecular mechanisms of bidirectional antagonism between K65R and thymidine analog mutations in HIV-1 reverse transcriptase.
 PMID: 17589186       2007       AIDS (London, England)
Abstract: In addition, the TAMs combination D67N/K70R/T215F/K219Q decreased susceptibility to the L-nucleotide lamivudine by a discrimination mechanism, whereas the M41L/L210W/T215Y combination had little effect on susceptibility to lamivudine.
Abstract: RESULTS: The addition of K65R to two clinically relevant combinations of TAMs (M41L/L210W/T215Y or D67N/K70R/T215F/K219Q) significantly reduced the recombinant enzymes' ability to excise all chain-terminating  PMID: 17668565       2007       Antiviral therapy
Abstract: The first case had an N42D mutation in the HR1 region of the gp41, along with transmitted resistance mutations in the protease (D30N, M361, N88D) and in the RT (M41L, L210W, T215D).


  Quadruple nucleoside therapy with zidovudine, lamivudine, abacavir and tenofovir in the treatment of HIV.
 PMID: 17713153       2007       Antiviral therapy
Abstract: The presence of L210W, or at least two of the mutations 41L, 67N, 70R, 215F/Y or 219Q/E, at or before baseline seems to be a predictor of non-response, whereas the presence of M184V does not impede virological response and might even be advantageous.


  Impact of the number of failed therapeutic regimes on the development of resistance mutations to HIV-1 in northeast Brazil.
 PMID: 17962868       2007       The Brazilian journal of infectious diseases
Abstract: There was a significant increase in resistance mutations V82A/F/L/T, I84V, L90M, M41L, K70R, L210W, T215Y/F and K219Q/E in MF.


  Improved interpretation of genotypic changes in the HIV-1 reverse transcriptase coding region that determine the virological response to didanosine.
 PMID: 18008248       2007       The Journal of infectious diseases
Abstract: The best correlation with response was found with the derived score (M41L x 2) + E44D/A/G + T69D/S/N/A + (L210W x 2) + T215Y or revertants + L228H/R - D123E/N/G/S, by use of which viruses were categorized as being susceptible (score < or =0), as having intermediate resistance (1-3), and as being resistant (> or =4) to didanosine.


  N348I in the connection domain of HIV-1 reverse transcriptase confers zidovudine and nevirapine resistance.
 PMID: 18052601       2007       PLoS medicine
Method: The M41L, L210W, T215Y, and N348I mutations were introduced into WT HIV-1LAI RT by site-directed mutagenesis using the QuikChange Mutagenesis kit.
Method: The analysis was performed for N348I and for each of the TAMs: M41L, D67N, K70R, L210W, T215Y/F, and K219Q/E.
Result: Because N348I is highly associated with TAMs (Figure 1), we also introduced N348I into molecular clones that contained M41L and T215Y (NL


  [Study on genotypic resistance mutations to antiretroviral drugs on HIV strains of treated and treatment-naive HIV-1 infectious patients in Hubei province].
 PMID: 18396668       2007       Zhonghua liu xing bing xue za zhi
Abstract: Some protease (PR) drug-resistant mutations were found in these samples, such as D30N (2.27%), D30G (2.27%), M46I (4.55%), M46N (2.27%), I47V (4.55%), I84V (4.55%), I84L (2.27%), N88S (2.27%) and L90S (2.27%) that all belonged to major drug-resistant but A71T (29.55%) belonged to minor resistance mutations Five treated patients were detected having mutations associated RT drug resistance: M41L (5.26%), A62V (5.26%),D67N (5.26%),  PMID: 16332398       2006       Virus research
Abstract: Principal antiretroviral resistance mutations (ARM) were observed in 3% of the samples, two cases with K103N and one with M41L, L210W and T215Y, all in HIV-1 clade B infected men.



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