Kusmartseva, I., Wu, W., Syed, F. et al. ACE2 and SARS-CoV-2 Expression in the Normal and COVID-19 Pancreas. This article is a preprint and has
Spotlight on Covid-19 Research Publications
Researchers aiming to block excessive lung inflammation in COVID-19 patients found upregulated immune checkpoint biomarkers in patients with a range of COVID-19 symptoms (from paucisymptomatic to acute respiratory distress syndrome). In addition, Carvelli et al found increased expression of C5a, an inflammatory mediator, in serum and the C5aR1 receptor on myeloid cells in COVID-19 patients, which are known to initiate inflammatory responses by recruiting naeutrophils and monocytes to lungs. An In vitro neutrophil migration assay quantified with the CytoNuclear FL Module of HALO software demonstrated that the clinical stage therapeutic monoclonal antibody, avdoralimab, effectively inhibited C5a-induced neutrophil migration. The authors propose use of avdoralimab to limit excessive lung inflammation associated with acute respiratory distress in COVID-19 patients.
Blair, R.V., Vaccari, M., Doyle-Meyers, L.A.. et al. Acute Respiratory Distress and Cytokine Storm in Aged, SARS-CoV-2 Infected African Green Monkeys, but not in Rhesus Macaques. This article is a preprint and has not been certified by peer review. doi: https://doi.org/10.1101/2020.06.18.157933. SARS-CoV-2 induces a wide range of disease severity ranging from asymptomatic infection, to a life-threating illness, particularly in the elderly and persons with comorbid conditions. Among those persons with serious COVID-19 disease, acute respiratory distress syndrome (ARDS) is a common and often fatal presentation. Animal models of SARS-CoV-2 infection that manifest severe disease are needed to investigate the pathogenesis of COVID-19 induced ARDS and evaluate therapeutic strategies.