HIV mutation literature information.


  Does GSS still maintain relevance on HAART outcome after the introduction of newest active antiretroviral drugs? 48 weeks results.
 PMID: 22211659       2011       Current HIV research
Abstract: About 60% of tests reported L10FIRVC, M36ILV, M46IL, I54VLAMTS, V82AFTSLI, and L90M mutations in the protease region.


  Presence of drug resistance mutations among drug-naive patients in Morocco.
 PMID: 21087198       2011       AIDS research and human retroviruses
Abstract: The presence of DRMs was found in four (5.06%) of 91 patients; resistance mutations to NRTIs were M184V and T215I/S revertant mutations; resistance to NNRTIs was associated with K103N and resistance to PIs with V82A.


  Differences in reversion of resistance mutations to wild-type under structured treatment interruption and related increase in replication capacity.
 PMID: 21297946       2011       PloS one
Introduction: Mixtures of wild-type and variants T215Y in RT, L10F, I54V and V82A in PR appeared 6 months after the first mixture at position 184 was detected.
Introduction: The authors reported a faster rate of reversion for primary resistance mutations (K70R, M184I/V, T215Y/F in RT, and D30N, M46I/L, V82A, L90M in PR) compared to secondary mutations (M41L, D67N,


  The L76V mutation in HIV-1 protease is potentially associated with hypersusceptibility to protease inhibitors Atazanavir and Saquinavir: is there a clinical advantage?
 PMID: 21314993       2011       AIDS research and therapy
Table: V82A


  Rapid development of antiretroviral drug resistance mutations in HIV-infected children less than two years of age initiating protease inhibitor-based therapy in South Africa.
 PMID: 21345162       2011       AIDS research and human retroviruses
Abstract: Of 41 children without virologic suppression with posttreatment HIV genotype data available, major resistance mutations were found in 32 (78%): 14 (36%) had PI mutations including V82A, M46I, and L90M; 29 (71%) had M184V/I; and three had NNRTI mutations (K103N, Y181C, and G190A).


  Genotypic prediction of resistant mutation in HIV-1 pol gene towards the antiretroviral drugs.
 PMID: 21441094       2011       International journal of bioinformatics research and applications
Abstract: Two sequences of protease show the major mutation with mutations sites of I54V and V82A and 8 sequences shown other mutations.


  Increase of transmitted drug resistance among HIV-infected sub-Saharan Africans residing in Spain in contrast to the native population.
 PMID: 22046345       2011       PloS one
Result: Among SSA, RT-M184I/V and PR-M46L were the most frequent mutations, respectively, meanwhile in both Spanish natives and CSA, RT-T215rev and PR-V82A were the most prevalent substitutions.


  Correlation between resistance profile and immunosuppression in heavily treated HIV-1 infected Romanian patients.
 PMID: 22180722       2011       Romanian biotechnological letters
Abstract: A significantly higher total number of mutations were encountered in severely immunosuppressed patients, who presented also major mutations in the protease gene (V82A, I54V, G48V) and the major M184V mutation associated with type 2 thymidine analogs mutations in reverstranscriptase gene.CONCLUSION: A good immune status seems to be associated with a low range of mutations, indicating the impact of immune restoration or preservation on the therapeutic success rate.
Result: Five out of the 21 patients with severe immunosuppression harbored major PI mutations V82A, I54V, and G48V associated with phenotypic resistance to ritonavir.


  Can linear regression modeling help clinicians in the interpretation of genotypic resistance data? An application to derive a lopinavir-score.
 PMID: 22110581       2011       PloS one
Result: Both the LASSO and the LAR/LASSO models only include a maximum of 3 main effects: pre-TCE viral load and mutation V82A (LAR) and pre-TCE viral load and mutations I54V and V82A (LASSO) as well as their interactions with viral load.
Result: The ASE was greatly reduced when pre-TCE viral load entered the model and additionally reduced when V82A entered the model.
Table: V82A


  In Vivo validation of a bioinformatics based tool to identify reduced replication capacity in HIV-1.
 PMID: 21603285       2010       The open medical informatics journal
Discussion: However, comparison is difficult due to the presence of different mutations in the HIV protease (D30N versus I54V+V82A), as well as the variability inherent in experiments employing SCID-hu mice in which a chimeric organ is created by engraftment of primary human tissues.
Discussion: Nonetheless, the differences in these results may also suggest that virus containing the D30N mutation is less able to replicate in the thymus than virus containing the V82A mutation (as is suggested by our bioinformatics model).
Discussion: who found that mice infected with a virus (210P) containing protease mutation at I54V and V82A had a higher level of viremia than mice infected w



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