This week, researchers identified the molecule that has allowed a novel human coronavirus to infect at least 14 people, killing eight, since its detection last year. This key discovery, which pinpoints the receptor that the virus uses to infect cells in the human airways, opens up opportunities to study the virus’s origin, the level of risk it poses and potential drugs and vaccines.
But it will take more than lab work to determine whether the virus is the next SARS — the coronavirus responsible for severe acute respiratory syndrome, which infected more than 8,000 people and killed more than 750 in the early 2000s — or just an exotic pathogen of little broad importance to public health. Only epidemiological data can show how efficiently the new coronavirus, hCoV-EMC, spreads from person to person and whether it is as deadly as it seems — such data are sorely lacking.
To jump to humans, animal viruses such as these novel coronaviruses, and avian and swine flu viruses, must evolve to be able to latch onto proteins on the surfaces of human cells. In a paper published this week in Nature, Stalin Raj at the Erasmus Medical Centre in Rotterdam, the Netherlands, and a largely European team report that spikes on the surface of hCoV-EMC bind to DPP4, a well-known receptor protein on human cells.
When the binding site for the virus on DPP4 was blocked using antibodies, the virus could not infect cells; conversely, when DPP4 was expressed on the surface of normally non-susceptible cells, hCoV-EMC could now infect them.
The authors “unequivocally demonstrate that DPP4 is the receptor”, says Ian Lipkin, a renowned virus hunter at Columbia University in New York. Although other receptors or co-receptors might be involved, the experiments suggest no need to look further, he says.
The work seems “solid and important”, adds Michael Farzan, a virologist at the Scripps Research Institute’s campus in Jupiter, Florida, who a decade ago led the team that discovered the receptor used by the SARS virus to enter human cells.