Smriti Mallapaty in Nature:
As the number of coronavirus infections approaches 100,000 people worldwide, researchers are racing to understand what makes it spread so easily. A handful of genetic and structural analyses have identified a key feature of the virus — a protein on its surface — that might explain why it infects human cells so readily. Other groups are investigating the doorway through which the new coronavirus enters human tissues — a receptor on cell membranes. Both the cell receptor and the virus protein offer potential targets for drugs to block the pathogen, but researchers say it is too early to be sure. “Understanding transmission of the virus is key to its containment and future prevention,” says David Veesler, a structural virologist at the University of Washington in Seattle, who posted his team’s findings about the virus protein on the biomedical preprint server bioRxiv on 20 February1. The new virus spreads much more readily than the one that caused severe acute respiratory syndrome, or SARS (also a coronavirus), and has infected more than ten times the number of people who contracted SARS.
To infect a cell, coronaviruses use a ‘spike’ protein that binds to the cell membrane, a process that’s activated by specific cell enzymes. Genomic analyses of the new coronavirus have revealed that its spike protein differs from those of close relatives, and suggest that the protein has a site on it which is activated by a host-cell enzyme called furin. This is significant because furin is found in lots of human tissues, including the lungs, liver and small intestines, which means that the virus has the potential to attack multiple organs, says Li Hua, a structural biologist at Huazhong University of Science and Technology in Wuhan, China, where the outbreak began. The finding could explain some of the symptoms observed in people with the coronavirus, such as liver failure, says Li, who co-authored a genetic analysis of the virus that was posted on the ChinaXiv preprint server on 23 February2. SARS and other coronaviruses in the same genus as the new virus don’t have furin activation sites, he says. 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”, says Gary Whittaker, a virologist at Cornell University in Ithaca, New York. His team published another structural analysis of the coronavirus’s spike protein on bioRxiv on 18 February3.