# Monitoring of virological response and acquired HIV-1 drug resistance among patients initiating antiretroviral therapy in the Centre Region of Cameroon

**Authors:** Bello Djoda, Jerome Fru-Cho, Patrick Achiangia Njukeng, Ezechiel Ngoufack Jagni Semengue, Patrick Valere Tsouh Fokou, Evariste Molimbou, Naomi-Karell Etame, Rodrigue Kamga Wouambo, Bauer Wilhelm, Christopher Dächert, Alain Nantchouang Megaptche, Maximilian Muenchhoff, Abel Wade, Stefanie Van Cleaf, Josef Eberle, Charles Fokounang, Joseph Fokam, Oliver Till Keppler, Oliver Bosnjak

PMC · DOI: 10.11604/pamj.2025.52.122.46773 · The Pan African Medical Journal · 2025-11-21

## TL;DR

This study monitored HIV treatment response and drug resistance in Cameroon, finding higher treatment failure in rural areas and common resistance patterns linked to current ART regimens.

## Contribution

The study provides insights into virological response and drug resistance patterns in both urban and rural Cameroonian settings, highlighting the need for improved ART access and potential regimen adjustments.

## Key findings

- Rural patients had a 4.6-fold higher risk of virological failure compared to urban patients.
- 62.5% of patients with unsuppressed viral load had HIV drug resistance, primarily to NRTI and NNRTI drugs.
- No major resistance mutations were found for integrase strand transfer inhibitors, suggesting INSTI-based ART could be effective.

## Abstract

despite the success of antiretroviral therapy (ART), the emergence of HIV drug resistance (HIVDR) remains a major threat in sub-Saharan Africa, where therapeutic options remain limited. With the goal of supporting ART response, we sought to monitor viral load (VL) response and acquired HIVDR emergence among patients initiating ART in the Cameroonian setting.

a facility-based cohort study was conducted from March 2016 to May 2021 in urban (Yaoundé) and rural (Obala) settings in the Centre Region of Cameroon. Included were recently diagnosed HIV individuals initiating ART at the level of the health facilities. VL was measured at three different time points. For those with unsuppressed viremia (>1000 copies/mL), genotyping for HIVDR was performed in the protease, reverse-transcriptase, and integrase gene regions, and interpreted using HIVdb.v9.1. Data were analyzed with p<0.05 considered significant. Time-to-event analysis (Kaplan-Meier and Cox regression) was used to identify determinants of virological failure.

overall, 87 newly diagnosed participants (50.6% from urban and 49.4% from rural) were enrolled. Median (interquartile range, IQR) age was 42 (34.0-50.5) years, sex ratio (F/M) was 3/2, and all participants initiated treatment with non-nucleoside reverse transcriptase inhibitor (NNRTI)-based ART regimen. At initiation, median VL was 34,000 (13,963-122,000) copies/mL; at T1 (~3 years after initiation), median VL dropped to 9,800 (4,700-30,500) copies/mL, and 17.2% (15/87) switched to protease inhibitor-based ART. At the end of the study (T2), 58.6% (51/87) had achieved undetectable VL (<40copies/mL), 3.4% had VL between 40-999 copies/mL, and 37.9% VL >1000 copies/mL. The proportion with virological failure was 9.1% (4/44) in the urban setting versus 67.4% (29/43) in the rural setting. Time-to-event analysis revealed that patients in the rural setting had a 4.6-fold higher risk of virological failure (hazard ratio (HR) = 4.60, 95% CI: 2.29-9.27). Among those with unsuppressed VL, overall rate of HIVDR was 62.5% (20/32), driven by the mutations: M184V (31.25%) for NRTI, K103N (18.75%) for NNRTI and M46I (9.30%) for PI/r, and 0% major resistance mutations to integrase strand transfer inhibitors (INSTI), without any significant disparity between urban and rural.

viral load monitoring reveals poor ART response in rural settings, which prompts the need for improving access to ART. Among those with unsuppressed VL, the burden and patterns of HIVDR are similar in both settings, likely due to the wide use of NNRTI-based ART. Viral susceptibility to INSTIs supports a possible switch to dolutegravir-based ART for optimal response.

## Full-text entities

- **Genes:** CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}, MLC1 (modulator of VRAC current 1) [NCBI Gene 23209] {aka LVM, MLC, VL}
- **Diseases:** RLS (MESH:D020920), AIDS (MESH:D000163), ADR (MESH:D000069279), viremia (MESH:D014766), failure (MESH:D051437), HBV co-infection (MESH:D006509), HIV (MESH:D015658), positive (MESH:D000377), hepatitis (MESH:D056486), ART (MESH:D016609), infected (MESH:D007239), HCV (MESH:D006526), VL (MESH:D014777)
- **Chemicals:** rilpivirine (MESH:D000068696), EFV (MESH:C098320), darunavir (MESH:D000069454), DTG (MESH:C562325), 3TC (MESH:D019259), elvitegravir (MESH:C509700), atazanavir/ritonavir (MESH:C000718687), bictegravir (MESH:C000620396), raltegravir (MESH:D000068898), TDF (MESH:D000068698), PI (MESH:D010716), atazanavir (MESH:D000069446), cabotegravir (MESH:C584914), lopinavir/ritonavir (MESH:C558899), r (MESH:D001120), NVP (MESH:D019829), lopinavir (MESH:D061466), INSTIs (-), abacavir (MESH:C106538), doravirine (MESH:C000592662), etravirine (MESH:C451734), AZT (MESH:D015215)
- **Species:** Human immunodeficiency virus 1 (no rank) [taxon 11676], Homo sapiens (human, species) [taxon 9606]
- **Mutations:** E157Q, V32I, Y115F, I50L, A98G, K103N, M184V, M46I, K103N, M184V, V82A, T97A, M46I, M184

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12920547/full.md

## References

34 references — full list in the complete paper: https://tomesphere.com/paper/PMC12920547/full.md

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Source: https://tomesphere.com/paper/PMC12920547