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The structure of the virus provides some clues about its success. In shape, it’s essentially a spiky ball. Those spikes recognize and stick to a protein called ACE2, which is found on the surface of our cells: This is the first step to an infection. The exact contours of SARS-CoV-2’s spikes allow it to stick far more strongly to ACE2 than SARS-classic did, and “it’s likely that this is really crucial for person-to-person transmission,” says Angela Rasmussen of Columbia University. In general terms, the tighter the bond, the less virus required to start an infection.

There’s another important feature. Coronavirus spikes consist of two connected halves, and the spike activates when those halves are separated; only then can the virus enter a host cell. In SARS-classic, this separation happens with some difficulty. But in SARS-CoV-2, the bridge that connects the two halves can be easily cut by an enzyme called furin, which is made by human cells and—crucially—is found across many tissues. “This is probably important for some of the really unusual things we see in this virus,” says Kristian Andersen of Scripps Research Translational Institute.

For example, most respiratory viruses tend to infect either the upper or lower airways. In general, an upper-respiratory infection spreads more easily, but tends to be milder, while a lower-respiratory infection is harder to transmit, but is more severe. SARS-CoV-2 seems to infect both upper and lower airways, perhaps because it can exploit the ubiquitous furin. This double whammy could also conceivably explain why the virus can spread between people before symptoms show up—a trait that has made it so difficult to control. Perhaps it transmits while still confined to the upper airways, before making its way deeper and causing severe symptoms. All of this is plausible but totally hypothetical; the virus was only discovered in January, and most of its biology is still a mystery.

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The new virus certainly seems to be effective at infecting humans, despite its animal origins. The closest wild relative of SARS-CoV-2 is found in bats, which suggests it originated in a bat, then jumped to humans either directly or through another species. (Another coronavirus found in wild pangolins also resembles SARS-CoV-2, but only in the small part of the spike that recognizes ACE2; the two viruses are otherwise dissimilar, and pangolins are unlikely to be the original reservoir of the new virus.) When SARS-classic first made this leap, a brief period of mutation was necessary for it to recognize ACE2 well. But SARS-CoV-2 could do that from day one. “It had already found its best way of being a [human] virus,” says Matthew Frieman of the University of Maryland School of Medicine.