Dornase Alfa as a Potential Treatment Option for SARS-CoV-2: In Vitro Insights Dornaz Alfa'nın SARS-CoV-2 İçin Potansiyel Bir Tedavi Seçeneği Olarak Kullanımı: İn Vitro Bulgular
Fabad Journal of Pharmaceutical Sciences, vol.51, no.1, pp.175-188, 2026 (Scopus)
- Publication Type: Article / Article
- Volume: 51 Issue: 1
- Publication Date: 2026
- Doi Number: 10.55262/fabadeczacilik.1777903
- Journal Name: Fabad Journal of Pharmaceutical Sciences
- Journal Indexes: Scopus, EMBASE, Health Research Premium Collection (ProQuest), Pharma Collection (ProQuest)
- Page Numbers: pp.175-188
- Keywords: Coronavirus disease 2019, dornase alfa, neutrophil extracellular traps, severe acute respiratory syndrome coronavirus 2
- Open Archive Collection: AVESIS Open Access Collection
- Acibadem Mehmet Ali Aydinlar University Affiliated: Yes
Abstract
The potential use of dornase alfa (DA) in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been widely discussed, yet its mechanisms remain insufficiently characterized. Here, we investigated whether DA modulates SARS-CoV-2 through multiple in vitro readouts, including viral infectivity, viral RNA integrity, spike-mediated entry, T-helper cytokine polarization, and neutrophil extracellular trap (NET) formation. DA at 30 U reduced viral infectivity (p < 0.05). Quantum dot-based quantitative flow cytometry showed that DA (10 U and 30 U) decreased viral internalization, consistent with spike-binding-mediated entry inhibition (p < 0.05). qRT-PCR and sequencing suggested altered integrity/fragmentation of naked viral RNA after exposure to 30 U DA (p < 0.05). Cytokine bead array analyses of viral peptide-stimulated lymphocytes indicated a shift toward a Th2-skewed response in the presence of DA (p < 0.05). In addition, fluorescence microscopy demonstrated that 30 U DA suppressed phorbol myristate acetate-induced NETosis in polymorphonuclear leukocytes. Overall, these findings provide preliminary, hypothesis-generating evidence that DA may modulate SARS-CoV-2-related responses via multiple mechanisms. Larger, adequately powered studies are needed to validate these findings. However, clinical efficacy and any potential prophylactic role require confirmation in appropriately designed in vivo and patient-based studies.