A significant breakthrough from an international team of scientists, under the University of Bristol’s guidance, might have just discovered what makes SARS-CoV-2 so intensely infectious and able to spread so fast among cells.
The team published the discovery in Science a few days ago. The article describes how the virus’s capacity to infect human cells can be decreased by inhibitors that block a recently discovered interaction between viruses and hosts, a potential basis for anti-viral treatment.
Compared to other coronaviruses responsible for common colds and mild respiratory symptoms, SARS-CoV-2 is extremely transmissive. Many scientists are still trying to figure out why SARS-CoV-2 rapidly infects organs outside of the respiratory system, like the brain and heart.
The study used various approaches to discover that SARS-CoV-2 Recognises a protein known as neuropilin-1 on human cells’ surface to support viral infection.
Dr. Yohei Yamauchi, Dr. Boris Simonetti, and Professor Peter Cullen, the principal authors of the study, stated:
“Could the Spike protein of SARS-CoV-2 associate with neuropilin-1 to aid viral infection of human cells? Excitingly, in applying a range of structural and biochemical approaches, we have been able to establish that the Spike protein of SARS-CoV-2 does indeed bind to neuropilin-1.”
“Once we had established that the Spike protein bound to neuropilin-1, we were able to show that the interaction serves to enhance SARS-CoV-2 invasion of human cells grown in cell culture. Importantly, by using monoclonal antibodies—lab-created proteins that resemble naturally occurring antibodies—or a selective drug that blocks the interaction, we have been able to reduce SARS-CoV-2’s ability to infect human cells,” they added.
Interestingly, scientists from the Technical University of Munich, Germany, and the University of Helsinki, Finland, have also discovered that neuropilin-1 helps SARS-CoV-2 cell entry and infectivity.