Introduction: Following the Stanford algorithm (mutation list), minor resistance mutations (L10F, V11I, K20TV, L23I, L33F, K43T, F53L, Q58E, A71IL, G73STCA, T74P, N83D, and L89V) are assumed to have ancillary roles such as compensation for lower efficiency of proteolysis caused by major mutations; major resistance mutations (V32I, M46IL, I47VA, G48VM, PMID: 35061671
2022
PloS one
Table: G73S
Phylogenetic and Drug-Resistance Analysis of HIV-1 Sequences From an Extensive Paediatric HIV-1 Outbreak in Larkana, Pakistan.
Result: Similarly, DRM PI:N88D, associated with resistance against protease inhibitors (PI), such as atazanavir/ritonavir, and tipranavir/ritonavir was observed in two treatment-experienced participants, while DRMs PI:M46L, PI:D30N, PI:N83D, PI:K43T, PI:G73S, PI:L33F were seen in one treatment-experienced individual each (Table 3).
Table: G73S
Highly drug-resistant HIV-1 protease reveals decreased intra-subunit interactions due to clusters of mutations.
Result: Non-active-site mutations in this region, such as A71V and G73S, have been shown to propagate changes to the catalytic site and provide cross-resistance for inhibitors.
Trend of HIV-1 drug resistance in China: A systematic review and meta-analysis of data accumulated over 17 years (2001-2017).
Abstract: PDR mutation to protease inhibitors was found to be low (only G73S; 2% according to the CPR tool).
Table: G73S
Discussion: On the other hand, V106A (Mutation in the RT region that confers resistance to NNRTIs), M114V and Y115F (Mutations in the RTs region that confer resistance to NRTIs) and G73S (Mutation in the PI region that confers resistance to PIs) were all detected for the first time.
HIV-1 reverse transcriptase and protease mutations for drug-resistance detection among treatment-experienced and naive HIV-infected individuals.
Result: Three minor HIV protease inhibitor-related mutations (L10I, L10V, and G73S) were also detected in four patients, although these mutations are not included in the WHO SDRMs list (Table 4).
Table: G73S
Transmission of HIV-1 drug resistance mutations within partner-pairs: A cross-sectional study of a primary HIV infection cohort.
Abstract: Two (14% [95% CI 1.8%-42.8%]) G73S accessory mutations were detected in both transmitter and recipient.
Result: In the first of our post-hoc analyses, in which we considered only the 25 partner-pairs in which the direction of transmission could be determined and used the 1% threshold, we observed one G73S in both the transmitter and recipient partner out of 13 low-frequency mutations identified in known transmitters (7.7%, exact 95% CI 0.19%-36.0%), with an expected likelihood of identifying one or more mutations in recipients of 32.3%.|mg
Table: G73S
Discussion: High-frequency mutations transmitted from ARV-naive partners likely represent transmission chains of drug-resistant variants, whereas there are alternate explanations for the presence of the G73S accessory mutation as minority variants in both transmitters and recipients.
Mechanism of Darunavir (DRV)'s High Genetic Barrier to HIV-1 Resistance: A Key V32I Substitution in Protease Rarely Occurs, but Once It Occurs, It Predisposes HIV-1 To Develop DRV Resistance.
Discussion: reported that 11 amino acid substitutions, V11I, V32I, L33F, I47V, I50V, I54L/M, G73S, L76V, I84V, and L89V, which appear to be associated with HIV-1 resistance against DRV, were identified among HIV-1 variants isolated from patients treated with DRV-including regimens on POWER studies.
Acquisition of tenofovir-susceptible, emtricitabine-resistant HIV despite high adherence to daily pre-exposure prophylaxis: a case report.
Result: SGS detected minor resistance mutations in the PR gene that were not reported in the standard genotype (D30N (3.6%), G73S (1.8%) and G48E (5.5%).
HIV mutation literature information.
PMID: 
2022
Scientific reports
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