DNA INTEGRITY IN ACUTE AND CHRONIC LONG COVID PATIENTS

Resumo

INTRODUCTION: Long COVID, also known as post-COVID-19 condition, encompasses a wide spectrum of persistent or delayed-onset symptoms following acute infection with SARS-CoV-2. These symptoms can be heterogeneous and multisystemic, persisting for weeks or months, yet the underlying pathophysiological mechanisms remain unclear. One hypothesis involves genomic instability caused by DNA damage, particularly oxidative lesions, which could contribute to symptom persistence. OBJECTIVE: To assess DNA integrity in individuals with acute and chronic long COVID compared to uninfected controls using the alkaline and enzyme-modified comet assays. METHODS: This cross-sectional study included 231 participants from Campo Bom (RS, Brazil), divided into three groups: control (n = 74), acute long COVID (symptoms 3–12 weeks; n = 79), and chronic long COVID (symptoms >12 weeks; n = 78). Peripheral blood samples were collected in heparin tubes and subjected to the standard alkaline comet assay and the enzyme-modified assay using formamidopyrimidine-DNA glycosylase (FPG), which detects oxidized purines such as 8-oxoGua. Slide analysis was performed using Comet Assay IV software. Statistical analysis was conducted using the nonparametric Mann–Whitney U test with significance set at p ≤ 0.05. RESULTS: In the standard comet assay, mean DNA damage percentages were 5.19 ± 0.26% (control), 5.05 ± 0.40% (acute), and 5.03 ± 0.39% (chronic), with no significant difference between groups (F = 0.460; p = 0.632). However, a sex-specific difference was noted, with males in the acute long COVID group exhibiting greater damage than females. All groups showed significantly increased damage after FPG treatment (p < 0.001), indicating the presence of oxidative lesions, but no intergroup differences were detected. CONCLUSION: Our findings reveal the presence of oxidative DNA damage in all participants, regardless of long COVID status, suggesting that persistent symptoms are not associated with increased genomic instability. These results underscore the need for further research into alternative mechanisms underlying long COVID pathophysiology.