literature

HIV mutation literature information.

Stereoselective synthesis and antiviral activity of D-2',3'-didehydro-2',3'-dideoxy-2'-fluoro-4'-thionucleosides.

PMID: 12383014 2002 Journal of medicinal chemistry

Abstract: Molecular modeling studies demonstrated that the larger van der Waals radius as well as the close proximity to Met184 of the 4'-sulfur atom of D-2'-F-4'-Sd4C (17) may be the reasons for the decreased antiviral potency of synthesized 4'-thio nucleosides against the lamivudine-resistant variants (HIV-1(M184V)).

Abstract: The cytidine 17 and 5-fluorocytidine 18 analogues showed significantly decreased antiviral activity against the clinically important lamivudine-resistant variants (HIV-1(M184V)), whereas the corresponding D-2'-Fd4 nucleosides showed limited cross-resistance.

Molecular mechanisms of resistance to human immunodeficiency virus type 1 with reverse transcriptase mutations K65R and K65R+M184V and their effects on enzyme function and viral replication capacity.

PMID: 12384348 2002 Antimicrobial agents and chemotherapy

Abstract: ATP-mediated removal of carbovir as well as small increases in the inhibitory capacity of carbovir appear to contribute to the resistance of mutants with the K65R mutation and the mutants with the K65R and M184V mutations to abacavir.

Abstract: Enzymatic and viral replication analyses were undertaken to elucidate the mechanisms of altered drug susceptibilities and potential fitness defects for the K65R and K65R+M184V mutants.

Abstract: Finally, both the HIV-1 K65R mutant and, more notably, the HIV-1 K65R+M184V double mutant showed reduced replication capacities and reduced RT processivities in vitro, consistent with a potential fitness defect in vivo and the low p

Interactions of enantiomers of 2',3'-didehydro-2',3'-dideoxy-fluorocytidine with wild type and M184V mutant HIV-1 reverse transcriptase.

PMID: 12406504 2002 Antiviral research

Abstract: Molecular modeling suggests that L- and D-D4FC-TP are positioned in the active site favorably for incorporation by RT(WT) and that L-D4FC-TP, but not D-D4FC-TP, is sterically hindered by the addition of a beta branched amino acid at position 184 of RT(M184V).

Abstract: The kinetic parameters of incorporation in the presence of L-D4FC-TP by RT(WT) and the mechanism of resistance by RT(M184V) were found to be distinct from those seen with the corresponding L-isomers containing an oxathiolane ring: (-)-3TC-TP and (-)-FTC-TP.

Abstract: While no resistance was conferred by the methionine 184 to valine mutation to D-D4FC-TP, L-D4FC-TP was incorporated 50- to 70-fold less efficiently.

The M184V mutation in HIV-1 reverse transcriptase reduces the restoration of wild-type replication by attenuated viruses.

PMID: 12461412 2002 AIDS (London, England)

Abstract: CONCLUSIONS: These findings provide further biological and biochemical evidence that M184V-containing viruses are impaired in replication fitness.

Abstract: METHODS: Viruses containing deletions in non-coding regions of the viral genome were examined in tissue culture to see whether the additional presence of M184V delays the reestablishment of wild-type replication kinetics.

Abstract: OBJECTIVE: To study the ability of HIV constructs containing the M184V substitution in reverse transcriptase (RT), which causes resistance to lamivudine, to evolve mutations that compensate for deletions within the HIV genome.

High prevalence of genotypic resistance to nucleoside reverse transcriptase inhibitors among therapy-naive individuals from the Warsaw cohort.

PMID: 12478325 2002 Infection

Abstract: In 54 (81.8%) out of 66 samples, a K70R mutation was identified, which was followed by an M184V mutation in 22 cases (33.3%).

Evolution of antiretroviral phenotypic and genotypic drug resistance in antiretroviral-naive HIV-1-infected children treated with abacavir/lamivudine, zidovudine/lamivudine or abacavir/zidovudine, with or without nelfinavir (the PENTA 5 trial).

PMID: 12553485 2002 Antiviral therapy

Abstract: Importantly, although in vitro, ABC selects for M184V as the first mutation, ABC did not select for M184V when combined with ZDV without 3TC.

Abstract: Reduced phenotypic susceptibility to ABC only occurred in the 3TC+ABC arm and required K65R and/or L74V in addition to M184V.

Might the M184V substitution in HIV-1 RT confer clinical benefit?

PMID: 12555696 2002 AIDS reviews

Abstract: Collectively, these factors might explain the residual antiviral effect and clinical benefit observed with continued use of 3TC in combination therapy regimens following the emergence of M184V.

Abstract: However, several of these trials did not possess adequate statistical power to resolve whether or not continued use of 3TC provided actual benefit, nor were they specifically designed to test the M184V benefit hypothesis in prospective fashion.

Abstract: Indeed, the results of numerous controlled as well as observational clinical studies are suggestive of improved therapeutic outcome associated with continued usage of 3TC and maintenance of the M184V mutation.

Prevalence of primary and secondary resistant mutations to antiretroviral drug in a population of Puerto Rican infected with HIV.

PMID: 12572241 2002 Puerto Rico health sciences journal

Abstract: Mutation frequencies to the NRTI ranged in appearance from as high as 54% (i.e., M184V) in the studied subjects to a low of less than 5% (i.e., M184I and V75T).

Molecular modeling approach to understanding the mode of action of L-nucleosides as antiviral agents.

PMID: 11120956 2001 Antimicrobial agents and chemotherapy

Abstract: Additionally, the clinically important M184V mutation, which confers resistance against 3TC and FTC, was studied with our modeling system.

Abstract: The binding energy patterns of nucleoside inhibitors at the M184V mutation site correlate with the reported antiviral data.

Analysis of HIV-1 mutation patterns in patients failing antiretroviral therapy.

PMID: 11170234 2001 Journal of clinical laboratory analysis

Abstract: The most frequent RT mutations were T215Y/F, M41L, and M184V (41.9, 40.8, and 40.8%, respectively), while L63P, L10R/V, and A71V/T (58, 41.9, and 34.4%, respectively) were the most represented protease substitutions.

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