Mucociliary transport deficiency and disease progression in Syrian hamsters with SARS-CoV-2 infection

Mucociliary transport deficiency and disease progression in Syrian hamsters with SARS-CoV-2 infection

Blog Article

Substantial clinical evidence supports the notion that ciliary function in the airways is important in COVID-19 pathogenesis.Although ciliary damage has been observed in both in vitro and in vivo models, esp sd-2 the extent or nature of impairment of mucociliary transport (MCT) in in vivo models remains unknown.We hypothesize that SARS-CoV-2 infection results in MCT deficiency in the airways of golden Syrian hamsters that precedes pathological injury in lung parenchyma.Micro-optical coherence tomography was used to quantitate functional changes in the MCT apparatus.Both genomic and subgenomic viral RNA pathological and physiological changes were monitored in parallel.

We show that SARS-CoV-2 infection caused a 67% decrease in MCT rate as early as 2 days postinfection (dpi) in hamsters, principally due to oas ba?adores 79% diminished airway coverage of motile cilia.Correlating quantitation of physiological, virological, and pathological changes reveals steadily descending infection from the upper airways to lower airways to lung parenchyma within 7 dpi.Our results indicate that functional deficits of the MCT apparatus are a key aspect of COVID-19 pathogenesis, may extend viral retention, and could pose a risk factor for secondary infection.Clinically, monitoring abnormal ciliated cell function may indicate disease progression.Therapies directed toward the MCT apparatus deserve further investigation.