# HIV-1 drug resistance and associated risk factors in patients with antiretroviral therapy failure in Chongqing, China, 2019–2023

**Authors:** Huizheng Zhang, Ping Wu, Wei Ye

PMC · DOI: 10.1371/journal.pone.0342301 · PLOS One · 2026-02-24

## TL;DR

This study finds high drug resistance in HIV patients in Chongqing, China, linked to low CD4 counts and initial use of certain drugs.

## Contribution

The study identifies key risk factors for HIV drug resistance in Chongqing and recommends optimized treatment strategies.

## Key findings

- 66.55% of patients with ART failure had HIV-1 drug resistance mutations.
- Lower baseline CD4+ T-cell counts and NNRTI-based regimens were independently associated with drug resistance.
- NNRTI resistance was most common, followed by NRTI resistance.

## Abstract

The emergence of drug resistance poses a major challenge to the long-term efficacy of antiretroviral therapy (ART) in managing HIV-1 infection. A comprehensive understanding of the prevalence and determinants of HIV-1 drug resistance mutations (DRMs) among patients with treatment failure in Chongqing, China, remains limited.

This study sought to characterize the prevalence of HIV-1 DRMs and to identify factors associated with drug resistance in patients experiencing ART failure in Chongqing between 2019 and 2023.

We conducted a retrospective analysis of individuals living with HIV/AIDS who had received ART for at least six months and exhibited virologic failure(VF) (viral load(VL) > 1000 copies/mL). Genotypic resistance testing was performed on plasma samples. Associations between potential risk factors and the presence of DRMs were evaluated using univariate and multivariate logistic regression models.

Of the 1,522 patients with ART failure included in the study, amplifiable partial pol and integrase (INT) gene sequences were obtained from 1,426 and 653 specimens, respectively. DRMs were identified in 66.55% (949/1,426) of the patients. The predominant HIV-1 subtype was CRF07_BC (50.14%). Class-specific DRM prevalence was highest for non-nucleoside reverse transcriptase inhibitors (NNRTIs) at 61.15%, followed by nucleoside reverse transcriptase inhibitors (NRTIs) at 44.60%, integrase strand transfer inhibitors (INSTIs) at 6.13%, and protease inhibitors (PIs) at 5.39%. The most commonly observed mutations were M184V/I (38.00%) for NRTIs, K103N/S/H (24.96%) for NNRTIs, and M46I (1.54%) for PIs. Multivariate analysis confirmed that lower baseline CD4 + T-cell counts and initiation of treatment with an NNRTI-based regimen were independently associated with the development of DRMs.

Our study reveals a high prevalence of HIV-1 drug resistance among patients with treatment failure in Chongqing, with low baseline CD4 + T-cell counts and NNRTI-based initial regimens identified as key risk factors. These findings underscore the urgency of optimizing first-line therapy by prioritizing dolutegravir (DTG)-based regimens, with protease inhibitor (PI)-based regimens as a practical alternative. Furthermore, we recommend implementing timely genotypic resistance testing, ideally within 4 weeks upon confirmed virologic failure, to guide effective regimen switching and curb the spread of drug resistance.

## Linked entities

- **Chemicals:** dolutegravir (PubChem CID 54726191)

## Full-text entities

- **Genes:** INTU (inturned planar cell polarity protein) [NCBI Gene 27152] {aka CPLANE4, INT, OFD17, PDZD6, PDZK6, SRTD20}, MLC1 (modulator of VRAC current 1) [NCBI Gene 23209] {aka LVM, MLC, VL}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, NFATC2 (nuclear factor of activated T cells 2) [NCBI Gene 4773] {aka JCOSL, NFAT1, NFATP}
- **Diseases:** death (MESH:D003643), toxicity (MESH:D064420), ART failure (MESH:D051437), VF (MESH:C537182), Resistance (MESH:D060467), opportunistic infections (MESH:D009894), DRMs (MESH:D000069279), AIDS (MESH:D000163), infectious diseases (MESH:D003141), HIV (MESH:D015658), DRM (MESH:C580316)
- **Chemicals:** TDF (MESH:D000068698), AZT (MESH:D015215), Integrase strand (-), ABC (MESH:C106538), Raltegravir (MESH:D000068898), NVP (MESH:D019829), Bictegravir (MESH:C000620396), lopinavir/ritonavir (MESH:C558899), EVG (MESH:C509700), 3TC (MESH:D019259), DTG (MESH:C562325), agarose (MESH:D012685), EFV (MESH:C098320), Cabotegravir (MESH:C584914), BIC (MESH:C100119), Emtricitabine (MESH:D000068679)
- **Species:** Homo sapiens (human, species) [taxon 9606], Human immunodeficiency virus 1 (no rank) [taxon 11676]
- **Mutations:** V75I, K238T/N, L10F, L74M, I54V, V179D/E, L90M, G118R, T215A, L74I, S147G, V106M/I, S68N, T97A, K103S, G163R, A128T, Y318F, E57Q, K219E/R, P225H, D67N, N348I, E44D, M41L, T69D, G140K, L234I, L76V, F116Y, G190A/S, L23I, N155H, Q95K, M46I, F77L, G48A, K103N/S, K101E/H, M230L, Q58E, M184V/I, Q151M, H51Y, K65R, M46I, K103R, L24I, K70E, L210W, I50V, V82A, L100I, K43T, K20T, K103N, F227L/C, A62V, L33F, K65R/N

## Full text

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## Figures

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## References

27 references — full list in the complete paper: https://tomesphere.com/paper/PMC12931755/full.md

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Source: https://tomesphere.com/paper/PMC12931755