literature

HIV mutation literature information.

Absence of resistance mutations in antiretroviral-naive patients treated with ritonavir-boosted saquinavir.

PMID: 16964832 2006 Antiviral therapy

Abstract: No major PRO mutations were detected, but 2/8 displayed single new minor PRO substitutions (M36I, L10I) at VF that were known or suspected not to have been present at baseline; both these substitutions exist as natural polymorphisms.

Characterization of drug-resistance mutations in HIV-1 isolates from non-HAART and HAART treated patients in Burkina Faso.

PMID: 16998878 2006 Journal of medical virology

Abstract: Among six HAART-treated patients, 6/6 and 3/6 had M36I and L63LP protease minor subtypes, respectively; and only two (33.33%) presented virus with K103N mutation.

Abstract: As expected, all patients presented the common (non-B subtype) M36I polymorphism and 26/29 (90%) the K20I mutation.

[Background study of HIV-1 drug resistant mutations in treatment-naive patients in liaoning province].

PMID: 17121220 2006 Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae

Abstract: Minor resistance mutation rate to protease inhibitors was 100%, including types of L63P (60.4%), V77I (60.4%), M36I/V (31.9%), A71V/T (22.0%), L10I (8.8%), and K20R (6.6%).

[Study of resistance using the TRUGENE HIV-1 genotyping system and analysis of agreement between rule-based algorithms and virtual phenotyping].

PMID: 15757587 2005 Enfermedades infecciosas y microbiologia clinica

Abstract: For the IP: key mutations L90M (26.1%), M46I (18.1%) and V82AFTS (12.9%); and accessory mutations L63P (50.5%), A71V (27.2%), L10I (25.2%) and M36I (19.2%).

Novel human immunodeficiency virus type 1 protease mutations potentially involved in resistance to protease inhibitors.

PMID: 15855527 2005 Antimicrobial agents and chemotherapy

Abstract: They never showed positive correlations with PI resistance mutations; if anything, H69N showed a negative correlation with the compensatory mutations M36I and L10I.

Subtype analysis and mutations to antiviral drugs in HIV-1-infected patients from Mozambique before initiation of antiretroviral therapy: results from the DREAM programme.

PMID: 15977236 2005 Journal of medical virology

Abstract: The pattern of covariation observed for K20R and D60E (but not L63P and M36I) was different between C and B subtype isolates from PR-inhibitor-treated patients.

Tipranavir: a ritonavir-boosted protease inhibitor.

PMID: 16060700 2005 Drugs

Abstract: Analysis of clinical isolates from treatment-experienced patients identified the following tipranavir resistance-associated HIV protease mutations: L10V, I13V, K20M/R/V, L33F, E35G, M36I, K43T, M46L, I47V, I54A/M/V, Q58E, H69K, T74P, V82L/T, N83D, I84V.

Selection and characterization of HIV-1 showing reduced susceptibility to the non-peptidic protease inhibitor tipranavir.

PMID: 16122817 2005 Antiviral research

Abstract: At the end of the selection experiments, viruses harbouring 10 mutations in the protease (L10F, I13V, V32I, L33F, M36I, K45I, I54V, A71V, V82L, I84V) as well as a mutation in the CA/SP1 gag cleavage site were selected and showed 87-fold decreased susceptibility to tipranavir.

Short communication. Antiretroviral drug resistance among drug-naive HIV-1-infected individuals in Djibouti (Horn of Africa).

PMID: 16312182 2005 Antiviral therapy

Abstract: The most frequent were secondary mutations associated with protease inhibitors (PIs): M36I, R41K and K20I/R.

Characterization of mutations in HIV type 1 isolates from 144 Cambodian recently infected patients and pregnant women naive to antiretroviral drugs.

PMID: 16386116 2005 AIDS research and human retroviruses

Abstract: According to the ANRS September 2004 list, polymorphism substitutions (>50% versus the subtype B consensus) of CRF01_AE at drug resistance positions were observed only in protease: I13V (81%), E35D (87%), M36I (100%), R41K (96%), and H69K (100%).

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