Clinical relevance of substitutions in the connection subdomain and RNase H domain of HIV-1 reverse transcriptase from a cohort of antiretroviral treatment-naive patients.
Result: However, HIV-1 protease mutations D30N and M36I that are responsible for resistance to NFV and HIV-1 RT D67N mutation that is responsible for AZT resistance eventually emerged.
Role of atazanavir in the treatment of HIV infection.
PMID: 19436623
2009
Therapeutics and clinical risk management
Introduction: Mutations more significant to be included in the GIQ model are the following: L10F/I/V, K20M/R, L24I, D30N, V32I, L33F, M36I/L, I47V/A, G48V, I50V, I50L, F53L, I54V/L/A/M/T/S, L63P, A71V/T, G73S, V77I, V82A/F/T, I84V, N88D/S and
HIV type-1 clade C resistance genotypes in treatment-naive patients and after first virological failure in a large community antiretroviral therapy programme.
Result: The most frequent protease mutations remained M36I (86%), L63P (60%), H69K (94%) and L89I/M (82%), similar to the consensus sequence noted for clade C (differing amino acids compared to clade B subtypes at positions M361, R41K, H69K AND L89M).
Result: The most frequent protease mutations were L89I/M (89%), H69K (88%), L63P (52%) and M36I (87%).
Discussion: The impact of these on viral drug susceptibility is uncertain, but many, including L10I/V, K20R
Virological efficacy and emergence of drug resistance in adults on antiretroviral treatment in rural Tanzania.
Abstract: Subtype specific secondary polymorphisms such as K20I and M36I in the PR were observed in almost all patients.
Genetic diversity and drug resistance of HIV type 1 circulating recombinant Form_BC among drug users in Guangdong Province.
PMID: 19698024
2009
AIDS research and human retroviruses
Abstract: The polymorphisms L19I, M36I, R41K, D60E, L63P, H69K, and I93L were complete substitutions, and were followed by T12S (94%), I15V (90%), and L89M (81%) separately.
Genotypic resistance profiles in antiretroviral-naive HIV-1 infections before and after initiation of first-line HAART: impact of polymorphism on resistance to therapy.
PMID: 18182278
2008
International journal of antimicrobial agents
Abstract: At baseline, the differences between CRF01_AE and B strain were mainly observed in the minor mutations L10I/V, M36I and L63P/I/H (P<0.001, chi(2)).
Multiple independent origins of a protease inhibitor resistance mutation in salvage therapy patients.
Introduction: Primary drug resistance mutations that alone confers moderate resistance such as V82A and L90M are initially selected followed by the addition of secondary mutations often located outside of the active site of the PR, such as L10I, M36I, M46I, L63P, or A71V leading to higher levels of resistance.
Drug resistance-associated genotypic alterations in the pol gene of HIV type 1 isolates in ART-naive individuals in North India.
PMID: 18240959
2008
AIDS research and human retroviruses
Abstract: Forty-nine percent had mutations in the hinge (M36I, R41K, H69K) and alpha-helix (L89M) regions of the C-virus protease, which has been linked to increased catalytic activity.
Clinically validated mutation scores for HIV-1 resistance to fosamprenavir/ritonavir.
PMID: 18390885
2008
The Journal of antimicrobial chemotherapy
Abstract: Two fosamprenavir/ritonavir mutation scores were constructed: score A (L10F/I/V + L33F + M36I + I54L/M/V/A/T/S + I62V + V82A/F/C/G + I84V + L90M) was based only on mutations associated with a worse VR, whereas score B (L10FIV + L33F + M36I + I54L/M/V/A/T/S + A71V - V77I - N88S + L90M) also took into account favourable mutations.
HIV mutation literature information.
PMID: 
2009
Antiviral research
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