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Updated: Aug 12, 2026
Rapid Screening of HIV Reverse Transcriptase and Integrase Inhibitors
Published on: April 9, 2014
Low Prevalence of Integrase Inhibitor Resistance Following Treatment Failure: A Real-World Analysis from Hunan
Xiaobai Zou1, Jinghang Zhang1, Wei Liu1
1STD, HIV/AIDS and Leprosy Prevention and Control, Hunan Provincial Center for Disease Control and Prevention, Changsha, Hunan, People's Republic of China.
Purpose:
With the global advancement of Global Combination Antiretroviral Therapy (cART) into the Integrase strand-transfer inhibitors (INSTIs) era, Human immunodeficiency virus (HIV) RNA virological suppression rates and treatment persistence have significantly improved due to the high efficacy and favorable tolerability of these agents. However, resistance to INSTIs, triggered by treatment failure for various reasons, is gradually increasing. The aim of this study was to assess the epidemiological characteristics, transmission dynamics of HIV INSTIs resistance mutations and their early warning value for regional prevention and control.
Patients And Methods:
Plasma samples were collected from patients in Hunan Province from January 2019 to December 2024, who were receiving INSTIs for at least 6 months, and experienced virological failure (viral load ≥1000 copies/mL). HIV-1 RNA quantitation and genotypic drug resistance testing were performed. Categorical variables were compared using Chi-square or Fisher's exact test. Statistical analyses were performed using R 4.5.3.
Results:
125 participants were enrolled, 72.00% were male, with a mean age of 51.84 ± 15.99 years. 60.00% had a CD4 count below 300 cells/μL and 41.60% had a viral load between 10,000-<100,000 copies/mL. Drug resistance mutations (DRMs) were detected in 5 patients (4.00%, 95% CI: 1.31-9.09%). The mutation rate was 1.64% (1/61, 95% CI: 0.04-8.80%) in the BIC-based regimens group and 6.78% (4/59, 95% CI: 1.88-16.46%) in the DTG-based regimens group. There was no statistically significant difference between the two groups (P = 0.203, Fisher's exact test). The detected mutations included G118R, L74M, E157Q, S230R, T66TA, S153F, and E157Q. A total of 15 transmission clusters were identified, with a network entry rate of 32.00% (40/125). Subtype G exhibited a significantly higher entry rate of 90.0% (9/10, 95% CI: 55.50-99.75%) compared to 26.96% (31/115, 95% CI:19.11-36.03%) for other subtypes combined (Fisher's exact test, P<0.001).
Conclusion:
This study indicates that resistance to INSTI after treatment failure is rare, with BIC exhibiting a higher genetic barrier than DTG. Nonetheless, given the potential for transmission of resistant variants, ongoing surveillance remains essential.
