Decoded | 'How novel coronavirus infection differs from that of SARS virus found'

Scientists have compared variants of the novel coronavirus and the closely related 2002-03 SARS pandemic virus and found the differences in their respective infection mechanisms, an advance that partly explains why COVID-19 transmission is much more difficult to control.

The findings, published in the journal Frontiers in Molecular Biosciences, noted that both the COVID-19 virus -- SARS-CoV-2 -- and the SARS coronavirus are very similar in sequence and almost identical in structure.

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However, compared to the SARS virus, which caused over 750 deaths and more than 8400 known cases of infection during the 2002-03 pandemic, the novel coronavirus has so far infected more than 103 million people across the world, killing over 2.25 million.

According to the scientists, including those from the University of Texas at El Paso in the US, some differences in the COVID-19 virus make it significantly more contagious.

"We found that because of mutations, the binding from SARS-CoV-2 to the human cell is much stronger compared with SARS-CoV," explained Lin Li, a co-author of the study from the University of Texas at El Paso.

Li believes the mutation could be one of the reasons why the novel coronavirus is spreading much faster and is difficult to control.

"SARS-CoV-2 also uses a much smarter strategy to attack the human cell than SARS-CoV," he said.

According to the scientists, when the SARS virus infects or binds to the human cell, it uses several key amino acid molecules, or residues, part of its proteins to do so.

In comparison, they said the novel coronavirus uses more such molecules, "making it more robust and easier to completely hijack the human cell."

"We identified the most important residues for SARS-CoV-2 to bind to the human cell. This type of data is key for drug development to cure or treat infections caused by these types of viruses," Li said.

The researchers also specifically analysed one of the main proteins in both the viruses -- the spike protein which enables them to infect cells.

They found that between the novel coronavirus and the SARS virus there is a change in mechanism of the section of the spike protein which binds to human cells.

"The binding domain needs to flip out so that it can bind to the human cell, but we found some strange mutations that happened. Like the hinge of a door, the binding domain may affect the flip mechanism of SARS-CoV-2," Li explained.

He believes this may make the virus more flexible, making it easier to bind to the human cell.

"This type of data is key for drug development to cure or treat infections caused by these types of viruses. These fundamental rules and features can also be used for future disease control when perhaps 10 years from now, there's a SARS-CoV-3 or 4," Li added.