Result: We observed 4 PI-associated RAMs in 6 children/adolescents, as follows: the combination mutation I54V + V82A (n = 2), M46I/M (n = 1), and I84I/V (n = 1).
Differences in human immunodeficiency virus-1C viral load and drug resistance mutation between plasma and cerebrospinal fluid in patients with human immunodeficiency virus-associated cryptococcal meningitis in Botswana.
Abstract: HIV-1 DRM discordance was found in 3/26 (11.5%); 1 had I84IT and another had M46MI in CSF only.
Result: Of these, one had HIV-1 strain harbouring I84IT and the other had M46MI protease inhibitor (PI)-associated mutation in CSF but not in the plasma.
Discussion: One participant had M46MI mutation and the other had I84IT.
Genotyping and antiretroviral drug resistance of human immunodeficiency Virus-1 in Jazan, Saudi Arabia.
Result: One patient had multiple resistance mutations to PI (V82A + I84IV, L01F + Q58E), and M184 V mutation to NRTI, he was genotype C and
Discussion: The most frequent mutations detected in this study were V82A + I84IV which are associated with PI conferring resistance to Atazanavir, Lopinavir, Lamivudine, Emtricitabine, Darunavir, and Abacavir.
Discussion: The mutations associated with resistance to PI were V82A + I84IV 1.8%, and L10F + Q58E 1.8%.
Treatment-Emergent Mutations and Resistance in HIV-Infected Children Treated with Fosamprenavir-Containing Antiretroviral Regimens.
Result: At VF, the following major treatment-emergent PI mutations or mutation mixtures were detected: M46M/I, I50I/V, I54I/M/V, and I84I/V, and the virus developed FPV RS.
The L33F darunavir resistance mutation acts as a molecular anchor reducing the flexibility of the HIV-1 protease 30s and 80s loops.
PMID: 29124158
2015
Biochemistry and biophysics reports
Introduction: L33F was initially identified as an accessory mutation to I54L/M, V32I+I47V, and I84V/I but is now recognized as a nonpolymorphic major drug resistance mutation.
Cobicistat-boosted darunavir in HIV-1-infected adults: week 48 results of a Phase IIIb, open-label single-arm trial.
Abstract: Of 15/313 patients who met the criteria for resistance analysis, one developed a darunavir RAM as a mixture with wild-type (I84I/V), without phenotypic resistance to darunavir.
Result: Only one of these 15 patients who was treatment experienced (prior antiretrovirals included efavirenz, emtricitabine, tenofovir disoproxil fumarate, zidovudine, lamivudine, stavudine) developed a resistance mutation to darunavir (at position I84 as a mixture with wild-type, I84I/V) (Table 4); this was not associated with phenotypic resistance to darunavir or other PIs.
Table:
Discussion: One of these 15 patients who was treatment experienced, developed a darunavir RAM at position I84 as a mixture with wild-type (I84I/V), which was not associated with phenotypic resistance to darunavir or other PIs.
Polymorphisms of HIV-2 integrase and selection of resistance to raltegravir.
Result: This variant outgrew an earlier transient variant harboring the I84I/R + L99L/I substitutions when cultured in the presence of 0.027 nM RAL, as well as the parental wild-type ROD strain when RAL concentration was increased to 0.082 nM.
Transmission networks of drug resistance acquired in primary/early stage HIV infection.
Result: In addition, cluster C represents an MDR transmission network, wherein all four PHIs harboured K103N and three of the four also harboured L10I, I54V, A71V, V82A/I/T, I84I/V, and L90M.
HIV mutation literature information.
PMID: 
2022
Antimicrobial agents and chemotherapy
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