Tianjiao Xue,1,2,* Tingting Liu,2– 5,* Yanfen Tang,1,2 Qi Chen,1,2 Yanyan Liu,1,2 Chenxi Cui,1,2 Chaohu Zhang,1,2 Jing Liu,1,2 Meng Zhang,1,2 Guifang Jin,1,2 Yuanyuan Zhang,2– 5 Yu Wang1,2 

1Department of Respiratory Medicine, Beijing Ditan Hospital, Capital Medical University, Beijing, People’s Republic of China; 2National Center for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, People’s Republic of China; 3Beijing Institute of Infectious Diseases, Beijing, People’s Republic of China; 4National Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, People’s Republic of China; 5Beijing Key Laboratory of Emerging Infectious Diseases, Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Yu Wang, Email dthx2025@outlook.com Yuanyuan Zhang, Email zhangyuanyuan@ccmu.edu.cn

Introduction: The advent of highly active antiretroviral therapy (HAART) has changed infection by human immunodeficiency virus (HIV) from an acute disease to a manageable chronic condition; however, pulmonary complications continue to affect patient quality of life. The goal of this research was to examine the link between CD4+ levels, viral load, and respiratory function in patients infected with HIV.
Methods: Patients were grouped as HIV-infected and non-infected (1:2 ratio). The analysis included between-group comparisons of the post-bronchodilator FEV1, FVC, FEV1/FVC ratio, forced expiratory flows at various lung volumes (FEF75, FEF50, FEF75/25), and carbon monoxide diffusion capacity (DLCO). We analyzed CD4+ counts and viral load effects on lung function using stepwise regression. For normally distributed continuous variables (presented as means ± SD), intergroup comparisons were performed using independent two-sample t-tests. Non-normal distributions (reported as medians [IQR]) were analyzed with Mann–Whitney U-tests. Categorical variables were compared using χ² or Fisher’s exact tests, with statistical significance set at p < 0.05.
Results: The study enrolled 150 participants infected with HIV with a mean age of 48 (39.25, 57.75) years; 87.33% were male and 46% had a history of smoking. The DLCO was significantly lower in patients with HIV (69.37 vs 82.23, p < 0.05) compared to patients without HIV. In patients with HIV, the DLCO was positively correlated with CD4+ T lymphocyte counts (r=0.5521, p < 0.0001) and negatively correlated with the HIV viral load (r=− 0.3942, p < 0.0001), and both were statistically significant. Patients with CD4+ ≥ 200 cells/μL had significantly higher VC (89.52 vs 79.31), FVC (91.80 vs 83.55), FEV1 (91.60 vs 84.40), and DLCO (74.61 vs 57.96) than those with CD4+ < 200 cells/μL. Similarly, patients with undetectable viral loads had higher VC (87.99 vs 81.08), FVC (90.90 vs 83.70), and DLCO (72.59 vs 60.62) than those with detectable viremia (all p < 0.05). The CD4+ count and FVC were significant predictors of the DLCO (p < 0.05).
Conclusion: HIV infection is significantly associated with impaired pulmonary diffusion function. Even after antiviral therapy when the viral load becomes undetectable (CD4+ T lymphocytes > 400), the impairment of pulmonary diffusion still persists. Therefore, we should strengthen the pulmonary function testing for AIDS patients, detect the risk of lung injury as early as possible, carry out timely interventions, and reduce the risk of chronic obstructive pulmonary disease (COPD).

Keywords: HIV infection, lung function, DLCO, CD4+ cell, pulmonary complications