1. SARS-CoV-2 binds to ACE2 receptors on motile cilia in airway epithelia, allowing it to traverse the mucus layer and access the cell body.
2. Depleting cilia blocks infection for SARS-CoV-2 and other respiratory viruses.
3. SARS-CoV-2 progeny attach to airway microvilli 24 hours post-infection, triggering formation of apically extended and highly branched microvilli that organize viral egress from the microvilli back into the mucus layer.
The article is generally reliable and trustworthy, as it provides a comprehensive overview of how SARS-CoV-2 penetrates the airway barrier of mucus and periciliary mucins to infect nasal epithelium. The article is well researched, with evidence provided from primary nasal epithelial organoid cultures, proteomics studies, kinase inhibition experiments, and other relevant research studies. The article does not appear to be biased or one sided in its reporting; rather, it presents both sides of the argument equally by exploring possible counterarguments and providing evidence for its claims. Furthermore, potential risks are noted throughout the article, such as how Omicron variants bind with higher affinity to motile cilia and show accelerated viral entry.
The only potential issue with this article is that it does not provide any missing points of consideration or missing evidence for its claims made; however, this is likely due to space constraints rather than any intentional omission on behalf of the authors. All in all, this article appears to be reliable and trustworthy in its reporting on SARS-CoV-2 replication in airway epithelia requiring motile cilia and microvillar reprogramming.