# HIV-1 drug resistance among HIV/HCV co-infected patients with treatment failure in Yunnan, southwestern China: a cross-sectional study

## TL;DR

This study found that HIV/HCV co-infected patients in Yunnan, China, had lower HIV drug resistance rates compared to HIV-only patients after treatment failure.

## Contribution

The study reveals distinct drug resistance patterns in HIV/HCV co-infected patients, especially in early treatment failure and immunodeficient individuals.

## Key findings

- HIV/HCV co-infected patients had a significantly lower drug resistance rate (37.5%) compared to HIV-only patients (55.0%).
- Co-infection was significantly associated with lower resistance in patients with 6–12 months of treatment and CD4+ count ≤ 350 cells/μL.
- The NRTI-related mutation T69D/N/S occurred less frequently in co-infected patients.

## Abstract

Yunnan Province remains a region with a high prevalence of human immunodeficiency virus (HIV) in China. Due to shared transmission routes, HIV/Hepatitis C virus (HCV) co-infection is common. This study aimed to analyze the prevalence and mutation patterns of HIV-1 drug resistance among HIV/HCV co-infected patients specifically following the virological failure of first-line highly active antiretroviral therapy (HAART) in Yunnan, and to compare these characteristics with HIV-1 mono-infected patients.

A cross-sectional study was conducted among 104 HIV/HCV co-infected and 120 HIV-1 mono-infected patients who experienced virological failure (HIV-RNA\geq 1,000 copies/mL) after at least 6 months of ART. Genotypic drug resistance was tested using an in-house method and analyzed via the Stanford HIV drug resistance database. Multivariable logistic regression and stratified analysis were performed to adjust for confounders.

Among patients with treatment failure, the drug resistance rate in the HIV/HCV co-infection group (37.5%) was significantly lower than in the HIV-1 mono-infection group (55.0%, P = 0.009). Multivariable logistic regression showed that HIV/HCV co-infection was associated with a lower trend of resistance, although it did not reach formal statistical significance after adjusting for gender, treatment duration, and CD4 + Count (aOR = 0.49, P = 0.084). However, stratified analysis revealed that co-infection was significantly associated with lower resistance in patients with a treatment duration of 6–12 months (OR = 0.24, P = 0.001) and those with CD4 + Count ≤ 350 cells/μL (OR = 0.38, P = 0.001). The frequency of the NRTI-related mutation T69D/N/S was significantly lower in the co-infected group (P = 0.029).

Among patients experiencing virological failure, HIV/HCV co-infection is associated with distinct genotypic resistance profiles, particularly in the early stages of treatment failure and among immunodeficient individuals. These findings suggest that co-infection status may influence the pathway to HIV drug resistance. Clinicians should prioritize prompt genotype resistance testing for co-infected patients failing ART to optimize second-line regimen adjustments.