Literature summary for 3.4.23.16 extracted from

Gonzalez, L.M.; Santos, A.F.; Abecasis, A.B.; Van Laethem, K.; Soares, E.A.; Deforche, K.; Tanuri, A.; Camacho, R.; Vandamme, A.M.; Soares, M.A.
Impact of HIV-1 protease mutations A71V/T and T74S on M89I/V-mediated protease inhibitor resistance in subtype G isolates (2008), J. Antimicrob. Chemother., 61, 1201-1204.

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Application

Application	Comment	Organism
medicine	isolation of subtype G viruses from patients with diverse amino acid combinations at codons 71, 74, 89 and 90. In isolates displaying 89I/V in combination with A71 or T74, a reversal to subtype G wild-type 89M is observed after growth in the absence of protease inhibitor. The presence of 71T in one isolate and 74S in another allows the persistence of 89I. Mutation 90M confers intermediate but significant degrees of drug resistance to ritonavir and nelfinavir in subtype G viruses. The combination of 71T or 74S, 89I and 90M results in higher levels of resistance to those protease inhibitors. 71T or 74S may stabilize 89I in the protease of subtype G	Human immunodeficiency virus 1

Protein Variants

Protein Variants	Comment	Organism
additional information	isolation of subtype G viruses from patients with diverse amino acid combinations at codons 71, 74, 89 and 90. In isolates displaying 89I/V in combination with A71 or T74, a reversal to subtype G wild-type 89M is observed after growth in the absence of protease inhibitor. The presence of 71T in one isolate and 74S in another allows the persistence of 89I. Mutation 90M confers intermediate but significant degrees of drug resistance to ritonavir and nelfinavir in subtype G viruses. The combination of 71T or 74S, 89I and 90M results in higher levels of resistance to those protease inhibitors. 71T or 74S may stabilize 89I in the protease of subtype G	Human immunodeficiency virus 1

Organism

Organism	UniProt	Comment	Textmining
Human immunodeficiency virus 1	-	subtype G	-

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Release 2023.1 (January 2023)