The Viral Fragment Theory of Covid-19 Vascular Complications
SARS-CoV-2 replication alone may not explain Covid-19.
One perplexing feature of Covid-19 is that it targets multiple organ systems despite being one type of virus. One answer to this oddity is that the coronavirus, SARS-CoV-2, exploits multiple receptors. The recent discovery of neuropilin-1 and CD147 (basigin) receptors — in addition to the previously known ACE2 receptor — explains why SARS-CoV-2 can invade the olfactory, pulmonary, vascular, and immune systems.
Another reason may be the virus’s capacity to inflame the blood vessels and cause clotting. As the blood vessels transverse all organs, vascular problems may have widespread health consequences. In line with this, a new theory has cast light on how SARS-CoV-2 might disturb the vascular system.
New findings
In a study published last month in Vascular Pharmacology, Yuichiro J. Suzuki, a professor at the Department of Pharmacology and Physiology at Georgetown University, and co-workers discovered that the spike protein of SARS-CoV-2 is enough to trigger a response in lab-cultured human endothelial and smooth muscle cells from the lungs’ blood vessels. Yes, just the spike protein, without the whole virion or its genome.
