literature

HIV mutation literature information.

Correlation between resistance profile and immunosuppression in heavily treated HIV-1 infected Romanian patients.

PMID: 22180722 2011 Romanian biotechnological letters

Discussion: I93L, found in two F1 patients from this study, one susceptible to all PIs and another one with low degree resistance to some of the class compounds is a secondary resistance mutation in subtype B that causes hyper susceptibility to PIs in subtype C isolates.

Prevalence of antiretroviral drug resistance mutations and HIV-I subtypes among newly-diagnosed drug-naive persons visiting a voluntary testing and counselling centre in northeastern South Africa.

PMID: 21957668 2011 Journal of health, population, and nutrition

Result: It differed from the global subtype B consensus at eight positions (T12S, I15V, L19I, M36I, R41K, H69K, L89M, and I93L).

Discussion: Several polymorphisms, such as K20R, M36I, and I93L, common in HIV-1 subtype C viruses and associated with drug resistance site, were also observed as has been previously reported.

Characterization of HIV type 1 subtype C protease gene: selection of L63P mutation in protease inhibitor-naive Indian patients.

PMID: 21453185 2011 AIDS research and human retroviruses

Abstract: Selection of T12S, I15V, L19I, M36I, R41K, H69K, L89M, and I93L was observed both in global and Indian subtype C while the L63P mutation was selected in Indian PR sequences.

Prevalence and clinical significance of HIV drug resistance mutations by ultra-deep sequencing in antiretroviral-naive subjects in the CASTLE study.

PMID: 20532178 2010 PloS one

Table: I93L

HIV drug resistance surveillance using pooled pyrosequencing.

PMID: 20174661 2010 PloS one

Table: I93L

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: Five high polymorphisms were found in CRF_07BC isolates; there were E35D (88%), R41K (100%), D60E (96%), L63P (99%), and I93L (91%).

Abstract: Four of the identified polymorphism positions (R41K, D60E, L63P, and I93L) were the same in the PR region of both subtypes.

Abstract: The polymorphisms L19I, M36I, R41K, D60E, L63P, H69K, and I93L were complete substitutions, and were followed by

Virological efficacy and emergence of drug resistance in adults on antiretroviral treatment in rural Tanzania.

PMID: 19583845 2009 BMC infectious diseases

Table: I93L

Differences in resistance mutations among HIV-1 non-subtype B infections: a systematic review of evidence (1996-2008).

PMID: 19566959 2009 Journal of the International AIDS Society

Abstract: The main differences are reflected in the discoveries that: (i) the non-nucleoside reverse transcriptase inhibitor resistance mutation, V106M, has been seen in subtype C and CRF01_AE, but not in subtype B, (ii) the protease inhibitor mutations L89I/V have been reported in C, F and G subtypes, but not in B, (iii) a nelfinavir selected non-D30N containing pathway predominated in CRF01_AE and CRF02_AG, while the emergence of D30N is favoured in subtypes B and D, (iv) studies on thymidine analog-treated subtype C infections from South Africa, Botswana and Malawi have reported a higher frequency of the K65R resistance mutation than that typically seen with subtype B.Additionally, some substitutions that seem to impact non-B viruses differentially a

Antiretroviral drug susceptibility among drug-naive adults with recent HIV infection in Rakai, Uganda.

PMID: 19276794 2009 AIDS (London, England)

Discussion: In one study, CRF02_AG isolates were more susceptible to nelfinavir and ritonavir than other subtypes (associated with K70R in protease); in the other study, subtype C isolates were hypersusceptible to lopinavir (associated with I93L).

Analysis and characterization of dimerization inhibition of a multi-drug-resistant human immunodeficiency virus type 1 protease using a novel size-exclusion chromatographic approach.

PMID: 19149765 2009 The Biochemical journal

Result: PRMDR contains multiple drug-resistant mutations (L10I, K45R, I54V, L63P, A71V, V82T, L90M and I93L) and is highly resistant to a number of active-site inhibitors, although it remains sensitive to the experimental active-site inhibitor JE-2147.

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