Monster or Machine? A Profile of the Coronavirus at 6 Months


Once upon a time, our pathogens were crudely named: Spanish flu, Asian flu, yellow fever, Black Death. Now we have H1N1, MERS (Middle East Respiratory Syndrome), H.I.V. — strings of letters as streamlined as the viruses themselves, codes for codes. The new coronavirus was temporarily named 2019-nCoV. On Feb. 11, the International Committee on Taxonomy of Viruses officially renamed it SARS-CoV-2, to indicate that it was very closely related to the SARS virus, another coronavirus.

Before the emergence of the original SARS, the study of coronaviruses was a professional backwater. “There has been such a deluge of attention on we coronavirologists,” said Susan R. Weiss, a virologist at the University of Pennsylvania. “It is quite in contrast to previously being mostly ignored.”

There are hundreds of kinds of coronaviruses. Two of them, SARS-CoV and MERS-CoV, can be deadly; four cause one-third of common colds. Many infect animals with which humans associate, including camels, cats, chickens, and bats. All are RNA viruses. Our coronavirus, like the others, is a string of roughly 30,000 biochemical building blocks called nucleotides enclosed in a membrane of both protein and lipid.

“I’ve always been impressed by coronaviruses,” said Anthony Fehr, a virologist at Kansas University. “They are extremely complex in the way that they get around and start to take over a cell. They make more genes and more proteins than most other RNA viruses, which gives them more options to shut down the host cell.”

The core code of SARS-CoV-2 contains genes for as many as 29 proteins: the instructions to replicate the code. One protein, S, provides the spikes on the surface of the virus and unlocks the door to the target cell. The others, on entry, separate and attend to their tasks: turning off the cell’s alarm system; commandeering the copier to make new viral proteins; folding viral envelopes, and helping new viruses bubble out of the cell by the thousands.

“I usually picture it as an entity that comes into the cell and then it falls apart,” Dr. Ott said. “It has to fall apart to build some mini-factories in the cell to reproduce itself, and has to come together as an entity at the end to infect other cells.”

For medical researchers, these proteins are key to understanding why the virus is so successful, and how it might be neutralized. For instance, to break into a cell, the S protein binds to a receptor called angiotensin converting enzyme 2, or ACE2, like a hand on a doorknob. The S protein on this coronavirus is nearly identical in structure to the one in the first SARS — “SARS Classic” — but some data suggests that it binds to the target enzyme far more strongly. Some researchers think this may partly explain why the new virus infects humans so efficiently.



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