Simulation of coronavirus formation is complete. The new coronavirus, which emerged in China in December 2019, has not only been spreading rapidly around the world, but also mutating. These characteristics make it difficult to predict the future course of the pandemic and to design effective vaccines and therapies. In light of these challenges, investigators have turned to modeling as a way to gain insights into the plausible mechanisms of the new coronavirus’s emergence and to forecast its future behavior.
The findings of these studies were published on February 11 in a special issue of the journal Viruses, which is devoted to early reports on the coronavirus pandemic. The simulations suggest that the new coronavirus arose through the recombination of two other coronaviruses—one that infects bats and one that infects humans—and that the resulting virus is well suited to infect both humans and bats.
The simulations also suggest that the new coronavirus is still evolving and that future outbreaks may be more severe than the current one. “Our findings underscore the need for continued surveillance and for the development of effective countermeasures,” says Trevor Bedford, a computational biologist at the Fred Hutchinson Cancer Research Center and one of the authors of the studies.
The studies are based on data from more than 4,000 whole-genome sequences of the new coronavirus that have been deposited in a database maintained by the Global Initiative on Sharing All Influenza Data (GISAID). Using this data, the authors reconstructed the evolutionary history of the new coronavirus and simulated its likely future evolution.
The first study, by Bedford and his colleagues, looked at the origins of the new coronavirus. The authors found that the new coronavirus is a recombinant of two other coronaviruses, one that infects bats and one that infects humans.
The bat coronavirus is closely related to a virus that was first isolated from a bat in 2013. The human coronavirus is closely related to the SARS-CoV virus that caused a global outbreak of respiratory illness in 2003.
The authors speculate that the new coronavirus might have first emerged in bats and then spread to humans through an intermediate host, such as a pangolin. (Pangolins are scaly, anteater-like creatures that are hunted for their meat and for their scales, which are used in traditional Chinese medicine.)
The second study, by Ralph Baric and his colleagues at the University of North Carolina at Chapel Hill, looked at the new coronavirus’s ability to spread from person to person.
The authors found that the new coronavirus is well suited to infect both humans and bats. In particular, the new coronavirus uses a protein called ACE2 to attach to and enter human cells.
ACE2 is found in the respiratory tract, which suggests that the new coronavirus is likely to spread through coughing and sneezing. The authors also found that the new coronavirus can infect cells that line the digestive tract, which suggests that it might be spread through fecal contamination.
Finally, the authors found that the new coronavirus has mutated in a way that makes it more infectious. Specifically, the virus has acquired a mutation in the spike protein that allows it to attach more tightly to human ACE2 receptors.
The authors conclude that the new coronavirus is still evolving and that future outbreaks may be more severe than the current one. “As the virus continues to evolve, we expect that it will become more efficient at infecting humans and causing disease,” Baric says.
A new study has produced the first model of the formation of the coronavirus. The work provides insights that could be useful for the development of therapeutics and vaccines against this virus and other respiratory illnesses.
The coronavirus is a spherical virus with a diameter of about 120 nanometers. It is composed of an outer shell of lipid (fat) molecules, and inside this shell are proteins that form a helical structure. This structure is called the nucleocapsid, and it contains the virus’s genetic material.
The new study, published in the journal Nature Communications, was led by University of Toronto professors Julio Monroy and Ravi Tumbalam. Using a technique called cryo-electron tomography, the researchers were able to image the three-dimensional structure of the coronavirus at a resolution of 3.5 nanometers.
This high-resolution structure allowed the researchers to create a model of the formation of the coronavirus. The model shows that the coronavirus is formed by the self-assembly of its components.
The lipid shell of the virus is made up of two types of molecules: those that form the membrane, and those that form the spikes that protrude from the surface of the virus. The membrane is made up of a lipid bilayer, with the spikes protruding through this bilayer.
The lipid molecules that make up the membrane are arranged in a specific way so that they can self-assemble into a sphere. The process begins with the lipid molecules forming a sheet. This sheet then folds in on itself to form a sphere, with the spikes protruding from the surface of the sphere.
The model shows that the coronavirus is assembled in a hierarchical manner, with the membrane forming first, followed by the assembly of the spikes. This hierarchical assembly is similar to the way that other viruses, such as influenza virus, are assembled.
The modeling work provides insights into the structure and assembly of the coronavirus. These insights could be useful for the development of therapeutics and vaccines against this virus and other respiratory illnesses.
