HIV type 1 integrase polymorphisms in treatment-naive and treatment-experienced HIV type 1-infected patients in Thailand where HIV type 1 subtype A/E predominates.
PMID: 21970343
2012
AIDS research and human retroviruses
Abstract: Major INI-RAM was not found in this study, but some minor INI-RAMs, such asV54I, L68I, L74M, T97A, and S230N, were found.
Drug resistance mutations of HIV type 1 non-B viruses to integrase inhibitors in treatment-naive patients from sub-saharan countries and discordant interpretations.
PMID: 22236055
2012
AIDS research and human retroviruses
Abstract: Using currently available interpretation algorithms (ANRS, HIVdb, and Rega), we identified the presence of mutations at nine resistance-associated positions including L74M (3.1%), T97A (9.3%), K156N (2.1%), E157Q (5.2%), G163K (1.0%), T206S (48.5%), S230N (1.0%), D232N (1.0%), and R236K (1.0%).
Study of genotypic and phenotypic HIV-1 dynamics of integrase mutations during raltegravir treatment: a refined analysis by ultra-deep 454 pyrosequencing.
PMID: 22238474
2012
The Journal of infectious diseases
Abstract: RESULTS: At baseline, primary resistance mutations were not detected by both population and UDPS genotypic assays; few secondary mutations (T97A-V151I-G163R) were rarely detected and did not show any statistically association either with virologic response at 24-weeks or with the development of resistant variants at failure.
BF integrase genes of HIV-1 circulating in Sao Paulo, Brazil, with a recurrent recombination region.
Result: Other B resistance-associated mutations were L74M (0.8%), T97A (1.6%), E138K (0.8%), M154I (3.9%), M154L (0.8%), E157K (2.3%), G163R (3.1%), and I203M (3.1%).
Genetic diversity and naturally polymorphisms in HIV type 1 integrase isolates from Maputo, Mozambique: implications for integrase inhibitors.
PMID: 22497664
2012
AIDS research and human retroviruses
Abstract: No major mutations conferring resistance to integrase inhibitors were found and polymorphic accessory mutations were solely observed in low frequency among subtype C sequences-L74M (3.4%), T97A (1.8%), and E157Q (1.8%)-suggesting that this new antiretroviral drug class will be effective in Mozambique providing a good perspective to the introduction of this class of drugs in that country.
In-vivo selection of the mutation F121Y in a patient failing raltegravir containing salvage regimen.
Abstract: At week 88 F121Y was no longer detected, L74I and T97A were maintained and Y143R emerged.
Abstract: The emergence of F121Y was observed at week 32 and 40, alongside with L74I, T97A, Q137H and V151I.
The activity of the integrase inhibitor dolutegravir against HIV-1 variants isolated from raltegravir-treated adults.
PMID: 22878423
2012
Journal of acquired immune deficiency syndromes (1999)
Abstract: The median fold change to dolutegravir for isolates containing changes at G140S + Q148H, G140S + Q148R, T97A + Y143R, and N155H (thus including raltegravir signature resistance codons) were 3.75, 13.3, 1.05, and 1.37, respectively.
Three main mutational pathways in HIV-2 lead to high-level raltegravir and elvitegravir resistance: implications for emerging HIV-2 treatment regimens.
Abstract: Collectively, our data define three major mutational pathways to high-level raltegravir and elvitegravir resistance: i) E92Q+Y143C or T97A+Y143C, ii) G140S+Q148R, and iii) E92Q+N155H.
Result: Collectively, these data show that raltegravir-resistant mutants of HIV-2 are cross-resistant to elvitegravir and that substitutions T97A+143C, Q148K/R, G140S+Q148R and E92Q+N155H confer high-level elvitegravir resistance in HIV-2.
Result: Dose-response profiles for variants
"Prolonged and substantial discordance in prevalence of raltegravir-resistant HIV-1 in plasma versus PBMC samples revealed by 454 ""deep"" sequencing."
Method: Secondary raltegravir-associated DRMs were defined to be E92V, Q95K, T97A, F121Y, E138A/K, G140A/C/S, S147G, V151A/I/L, M154I/L, E157Q, and G163K/R, and linkages examined were T97A and Y143C/R, E138A/K and Q148H/K/R, G140S and Q148H/K/R, and G163K/R and
HIV-1 integrase resistance among antiretroviral treatment naive and experienced patients from Northwestern Poland.
Result: In 14 cases with virologic success accessory mutations were present prior to the raltegravir introduction (11 sequences with E157Q, one of each L68V/E157Q, T97A, V151I).
Result: Other mutations and polymorphisms observed only in subtype B integrase sequences were L68V, T97A and V151I, while in non-B sequences R263K, E138D, L68IL and L74IL variants were noted (Figure 1b, Table 1).