Researchers Discover a Second 'Key' That Makes The New Coronavirus So Infectious

Researchers Discover a Second ‘Key’ That Makes The New Coronavirus So Infectious


23 OCTOBER 2020

It’s been 17 years since the coronavirus SARS-CoV threatened to erupt into a global pandemic. Thanks to rapid efforts to contain outbreaks of the infection, the world’s population was spared the worst.

This time we weren’t so fortunate. Just what makes SARS-CoV-2 so much more infectious than its predecessor is a question we’re now a little closer to solving, with researchers uncovering yet another way the virus gains entry into our cells.

Researchers from the Technical University of Munich in Germany and the University of Helsinki in Finland led a study that discovered a receptor called neuropilin-1 gives the novel coronavirus a leg-up in infecting our tissues.

This particular protein is relatively abundant on cells lining the nasal cavity, making it a piece of cake for the virus to establish a home inside our bodies, raise a virus family, and then spread to a new host.

Earlier this year it was discovered that a receptor called angiotensin-converting enzyme 2 (ACE2) helps the coronavirus bind to the surface of cells, while an enzyme called Type II transmembrane serine protease (TMPRSS2) is crucial for it gaining entry.

This kind of molecular lock-picking does a good job of explaining why both SARS coronaviruses wreak havoc throughout a range of tissues in our bodies, from the lining of our lungs to our digestive tract.

But it doesn’t say why one of the viruses does a better job of spreading than the other.

“The starting point of our study was the question why SARS-CoV, a coronavirus that led to a much smaller outbreak in 2003, and SARS-CoV-2, spread in such a different way even if they use the same main receptor ACE2”, says University of Helsinki virologist Ravi Ojha.

A crucial piece of the puzzle appeared on comparing the two viral genomes; SARS-CoV-2 had picked up sequences responsible for producing a prickly array of ‘hooks’, not unlike those used by other nasty pathogens to grip onto host tissues.

“Compared to its older relative, the new coronavirus had acquired an ‘extra piece’ on its surface proteins, which is also found in the spikes of many devastating human viruses, including Ebola, HIV, and highly pathogenic strains of avian influenza, among others,” . . .

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