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 HIV mutation literature information.


  Quasispecies variant dynamics during emergence of resistance to raltegravir in HIV-1-infected patients.
 PMID: 19221102       2009       The Journal of antimicrobial chemotherapy
Abstract: In most patients, raltegravir failure is associated with mutations in the IN gene, through two different genetic pathways: 155 (N155H) or 148 (Q148K/R/H).
Abstract: In the two patients switching from the 155 to the 148 pathway, clonal analysis showed that Q148R/H and N155H mutations were present on different strands, suggesting that these two pathways are independent.


  Lack of primary mutations associated with integrase inhibitors among HIV-1 subtypes B, C, and F circulating in Brazil.
 PMID: 19262402       2009       Journal of acquired immune deficiency syndromes (1999)
Abstract: Major mutations associated with elvitegravir or raltegravir in vivo resistance (Q148K/H/R, N155H) were not detected.


  Characterization and structural analysis of HIV-1 integrase conservation.
 PMID: 19290031       2009       AIDS reviews
Abstract: All primary signature mutations emerging in patients failing raltegravir (Y143R, Q148H/K/R, N155H) or elvitegravir (T66I, E92Q, S147G, Q148H/K/R, N155H), as well as secondary mutations (H51Y, T66A/K, E138K, G140S/A/C, Y143C/H, K160N, R166S, E170A, S230R, D232N, R263K) were complete


  Genetic barriers for integrase inhibitor drug resistance in HIV type-1 B and CRF02_AG subtypes.
 PMID: 19320246       2009       Antiviral therapy
Abstract: CONCLUSIONS: The major IN mutations E92Q, Q148K/R/H, N155H and E157Q (implicated in the resistance of IN inhibitors RAL and EVG) are highly conserved between subtypes B and CRF02_AG and display a similar genetic barrier.


  Virological and immunological response in HIV-1-infected patients with multiple treatment failures receiving raltegravir and optimized background therapy, ANRS CO3 Aquitaine Cohort.
 PMID: 19336453       2009       The Journal of antimicrobial chemotherapy
Abstract: Raltegravir-related mutations emerged in 9 of 11 failing patients (82%): Q148H/R (n = 5), N155S/H (n = 3) and S230N (n = 1).


  Evolution of raltegravir resistance during therapy.
 PMID: 19447792       2009       The Journal of antimicrobial chemotherapy
Abstract: The Q148R/H was detected only in subtype B.
Abstract: The Q148R/H was mostly detected after short exposure to raltegravir, while the Y143R was observed only after prolonged raltegravir exposure.
Abstract: The primary mutations N155H, Q148R/H or Q143R were observed during raltegravir therapy.


  The dynamics of appearance and disappearance of HIV-1 integrase mutations during and after withdrawal of raltegravir therapy.
 PMID: 19571721       2009       AIDS (London, England)
Abstract: Mutations Q148R (2 months) followed by G140A/Q148R and then G140A/Y143CHR/Q148R/G163R were detected in the virus from one patient, and these reverted to wild type when treatment was withdrawn, although clonal analysis identified maintenance of RAL resistance minority species at this time point.


  Selective-advantage profile of human immunodeficiency virus type 1 integrase mutants explains in vivo evolution of raltegravir resistance genotypes.
 PMID: 19605484       2009       Journal of virology
Abstract: After prolonged viral escape, mutants of the N155H pathway are replaced by mutants of the Q148HKR pathway.
Abstract: The emergence of human immunodeficiency virus type 1 resistance to raltegravir, an integrase strand transfer inhibitor, follows distinct and independent genetic pathways, among which the N155H and Q148HKR pathways are the most frequently encountered in treated patients.
Abstract: This finding likely explains why N155H can be selected early in the course of RAL resistance evolution in vivo but is later replaced by genotypes that include Q148HKR.


  HIV-1 IN alternative molecular recognition of DNA induced by raltegravir resistance mutations.
 PMID: 19623602       2009       Journal of molecular recognition
Abstract: Virologic failure during treatment with raltegravir, the first effective drug targeting HIV integrase, is associated with two exclusive pathways involving either Q148H/R/K, G140S/A or N155H mutations.


  Loss of raltegravir susceptibility by human immunodeficiency virus type 1 is conferred via multiple nonoverlapping genetic pathways.
 PMID: 19759152       2009       Journal of virology
Abstract: Both N155H and Q148R(H)(K) mutations reduced the replication capacity, while the addition of secondary mutations either improved or reduced the replication capacity depending on the primary mutation.
Abstract: Clonal analysis demonstrated that N155H and Q148R(H)(K) occur independently, not in combination.
Abstract: The human immunodeficiency virus type 1 (HIV-1) integrase mutations N155H and Q148R(H)(K) that reduce susceptibility to the integrase inhibitor raltegravir have been identified in patients failing treatment regimens containing raltegravir.



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