Why SARS-CoV-2 Is Spreading Much Faster Than SARS-CoV

The number of COVID-19 cases have surged exponentially worldwide in the past week. As of March Thursday, 509,427 cases and 23,004 deaths have been reported globally. 

The SARS-CoV-2’s fast spreading nature has raised some concerns among scientists since they are running short of time to curb its proliferation. Researchers have noted a difference between the speed at which SARS-CoV (virus behind SARS) reached the world and the rapidity of the current pandemic. 

It took eight months for SARS to infect 8,098 people and cause 774 deaths in 2003 with a 10 percent case fatality ratio, which is a huge contrast to the numbers being recorded presently. Earlier, SARS was considered the first pandemic of the 21st century, but COVID-19 has surpassed its magnitude in almost three months. 

By studying commonalities and differences between the SARS-CoV and SARS-CoV-2, several researchers have attempted to understand the structure of the virus, so as to contain its spread and find a vaccine. 

What Makes COVID-19 Spread Fast

Together, a certain key protein on the virus’ surface and a particular receptor in human cells enable the virus to move quickly. Since both SARS-CoV and SARS-CoV-2 share 86 percent of identical DNA sequencing, the comparisons are inevitable. 

The shape of the virus resembles a spiky ball, which has a particular site that when activated by certain enzymes, binds to human cell membranes. The enzyme called furin is present on the liver, lungs and intestines, which indicates that the virus could infect many organs. 

SARS virus A SARS coronavirus is seen in this undated handout photograph. REUTERS/Health Protection Agen

However, the difference is that the furin activation site “sets the virus up very differently to SARS, in terms of its entry into cells, and possibly affects virus stability and hence transmission,” as per Professor Gary Whittaker, a virologist at Cornell University, whose paper on COVID-19 needs peer-reviewing. 

When SARS-COV-2 was compared to avian influenza viruses, a protein called haemagglutinin was observed. It is similar to the spike-like proteins found in the novel coronavirus, which is why both viruses are widespread. 

The receptor that protein binds to is called angiotensin-converting enzyme 2 (ACE2), which is found on the surface of human cells. SARS-CoV-2’s spikes bind strongly to ACE2, much more tightly than SARS-CoV can. The stronger the ability to bind, the easier it is to infect the cells. “It’s likely that this is really crucial for person-to-person transmission,” Angela Rasmussen, of Columbia University, speculated.  

Another hypothesis is that SARS-CoV-2 enters both the upper and lower respiratory airways with the help of furin that is on all organs. This is probably why the virus jumps so quickly between people, even before symptoms are displayed. 

Till the scientists figure out the virus’ mechanism and find a vaccine, our safest bet is social distancing for now. 

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