The COVID-19 outbreak that emerged in China has infected millions of people and killed thousands worldwide. Public health authorities are racing for the pathogen to be suppressed, but this is not the first time the planet has had to combat a modern coronavirus outbreak. Here’s how the present scenario relates to previous epidemics.
The latest coronavirus was first documented in Wuhan, China, triggering a disease named COVID-19. It has now expanded to over 190 nations, including Japan, Italy, Iran, South Korea, and the United States.
The virus origins have not been verified, although early genetic research indicates that the pathogen emerged in bats and was then transmitted to an intermediary species before spilling into humans.
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LANDOVER, MARYLAND – MARCH 30: Healthcare professionals prepare to screen people for the coronavirus at a testing site erected by the Maryland National Guard in a parking lot at FedEx Field March 30, 2020 in Landover, Maryland. The guard, in cooperation with the state of Maryland and Prince Georges County, said the site will be able to test about 100 people a day for COVID-19 if they have been recommended by a doctor. There has been 1413 confirmed cases of coronavirus in Maryland and 15 deaths since the start of the global pandemic.
What makes COVID-19 more dangerous than these two?
Latest experiments have shown that the SARS-CoV-2 spike protein is highly adapted for human ACE2 binding. Simulations of viral binding of various species to homologous ACE2 proteins demonstrated the preference for bats and human ACE2.
The initial preprint of the researchers’ manuscript, made accessible online in March, was one of the first to computationally examine the high affinity or propensity of SARS-CoV-2 to bind with human ACE2.
“Beyond explaining the molecular mechanism of binding with ACE2, we also explored changes in the virus spike that could change its affinity with human ACE2,” said researchers said.
The SARS-CoV-2 protein spike attachment to ACE2, situated in the upper respiratory tract and acts as an entry point for other coronaviruses, like SARS, was computer-modeled by the researchers. The team used a molecular simulation technique to compute the binding power and interactions of the viral protein’s connection to ACE2.