HIV mutation literature information.


  Prevalence and pattern of drug resistance mutations among antiretroviral-treated HIV-1 patients with suboptimal virological response in Malaysia.
 PMID: 16404607       2006       Medical microbiology and immunology
Abstract: A patient with Q151M mutation complex was also detected.


  In vitro antiretroviral activity and in vitro toxicity profile of SPD754, a new deoxycytidine nucleoside reverse transcriptase inhibitor for treatment of human immunodeficiency virus infection.
 PMID: 16436719       2006       Antimicrobial agents and chemotherapy
Abstract: Insertions at amino acid position 69 and Q151M mutations (with or without M184V) reduced SPD754 susceptibility 5.2-fold and 14- to 16-fold, respectively (these changes gave values comparable to or less than the corresponding values for zidovudine, lamivudine, abacavir, and didanosine).


  Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
 PMID: 16440988       2006       Nucleosides, nucleotides & nucleic acids
Abstract: In this study, we measured the antiviral activity of FTC and 3TC against HIV-1 containing K65R, Q151M, and K65R/Q151M mutations.
Abstract: Overall, this study demonstrated that K65R and K65R/Q151M related drug resistance to FTC and 3TC was mainly due to a significant decrease in the rate of incorporation.
Abstract: The double mutation K65R/Q151M has been shown to be more resistant to many NRTIs than either of the single mutations alone.


  Virologic and enzymatic studies revealing the mechanism of K65R- and Q151M-associated HIV-1 drug resistance towards emtricitabine and lamivudine.
 PMID: 16440988       2006       Nucleosides, nucleotides & nucleic acids
Abstract: The Q151M mutation confers reduced susceptibility to many of the approved anti-HIV nucleoside analogues with the exception of 3TC and tenofovir.
Abstract: The Q151M mutation remained sensitive to both FTC and 3TC in both cell culture and enzymatic assays.


  The calculated genetic barrier for antiretroviral drug resistance substitutions is largely similar for different HIV-1 subtypes.
 PMID: 16540937       2006       Journal of acquired immune deficiency syndromes (1999)
Abstract: An increased genetic barrier was calculated for I82A (subtypes C and G), V108I (subtype G), V118I (subtype G), Q151M (subtypes D and F), L210W (subtypes C, F, G, and CRF02_AG), and P225H (subtype A) (P < 0.001 compared with subtype B).


  Clinical and genotypic correlates of mutation K65R in HIV-infected patients failing regimens not including tenofovir.
 PMID: 16555278       2006       Journal of medical virology
Abstract: However, exposure to abacavir and/or efavirenz, presence of Q151M and/or L100I, and prior AIDS may favor the selection of this mutation.


  Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
 PMID: 16555278       2006       Journal of medical virology
Abstract: Among genotypic correlates, the presence of M184V and NAMs seems to be protective for the emergence of K65R, while a strong positive correlation was found with the Q151M complex mutation.


  Prevalence of M184V and K65R in proviral DNA from PBMCs in HIV-infected youths with lamivudine/emtricitabine exposure.
 PMID: 16641288       2006       Journal of virology
Abstract: Among samples with K65R, a strong negative association was evident with the TAMs M41L, D67N, L210W, T215Y/F, and K219Q/E (P<0.005) but not with other NRTI mutations, including the Q151M complex.


  Insertions and deletions in HIV-1 reverse transcriptase: consequences for drug resistance and viral fitness.
 PMID: 16724949       2006       Current pharmaceutical design
Abstract: in the presence of Q151M), the effects of the deletion are not fully understood.


  Evidence of differential selection of HIV-1 variants carrying drug-resistant mutations in seroconverters.
 PMID: 16759049       2006       Antiviral therapy
Abstract: Among the mutations not detected in viruses from SCs, the RT E44D, V1081, Q151M and Y188C/H/L, and the protease D30N, G48V and V82A/F/S/T substitutions appeared to be negatively selected.



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