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

A virus, at heart, is information, a packet of data that benefits from being shared.


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

A virus, at heart, is information, a packet of data that benefits from being shared.

The information at stake is genetic: instructions to make more virus. Unlike a truly living organism, a virus cannot replicate on its own; it cannot move, grow, persist or perpetuate. It needs a host. The viral code breaks into a living cell, hijacks the genetic machinery and instructs it to produce new code — new virus.

President Trump has characterized the response to the pandemic as a “medical war,” and described the virus behind it as, by turns, “genius,” a “hidden enemy” and “a monster.” It would be more accurate to say that we find ourselves at odds with a microscopic photocopy machine. Not even that: an assembly manual for a photocopier, model SARS-CoV-2.

For at least six months now, the virus has replicated among us. The toll has been devastating. Officially, more than six million people worldwide have been infected so far, and 370,000 have died. (The actual numbers are certainly higher.) The United States, which has seen the largest share of cases and casualties, recently surpassed 100,000 deaths, one-fourth the number of all Americans who died in World War II. Businesses are shuttered — in 10 weeks, some 40 million Americans have lost their jobs — and food banks are overrun. The virus has fueled widespread frustration and exposed our deepest faults: of color, class and privilege, between the deliverers and the delivered to.

Still, summer — summer! — has all but arrived. We step out to look, breathe, vent. The pause is illusory. Cases are falling in New York, the epicenter in the United States, but firmly rising in Wisconsin, Virginia, Alabama, Arkansas, North and South Carolina,other states and many other countries around the world. China, where the pandemic originated, and South Korea saw recent resurgences. Health officials fear another major wave of infections in the fall, and a possible wave train beyond.

There may be trillions of species of virus in the world. They infect bacteria, mostly, but also abalone, bats, beans, beetles, blackberries, cassavas, cats, dogs, hermit crabs, mosquitoes, potatoes, pangolins, ticks and the Tasmanian devil. They give birds cancer and turn bananas black. Of the trillions, a few hundred thousand kinds of viruses are known, and fewer than 7,000 have names. Only about 250, including SARS-CoV-2, have the mechanics to infect us.

In our information age, we have grown familiar with computer viruses and with memes going viral; now here is the real thing to remind us what the metaphor means. A mere wisp of data has grounded more than half of the world’s commercial airplanes, sharply reduced global carbon emissions and doubled the stock price of Zoom. It has infiltrated our language — “social distancing,” “immunocompromised shoppers” — and our dreams. It has postponed sports, political conventions, and the premieres of the next Spider-Man, Black Widow, Wonder Woman and James Bond films. Because of the virus, the U.S. Supreme Court renders rulings by telephone, and wild boars roam the empty streets of Barcelona.

It also has prompted a collaborative response unlike any our species has seen. Teams of scientists, working across national boundaries, are racing to understand the virus’s weaknesses, develop treatments and vaccine candidates, and to accurately forecast its next moves. Medical workers are risking their lives to tend to the sick. Those of us at home do what we can: share instructions for how to make a surgical mask from a pillowcase; sing and cheer from windows and doorsteps; send condolences; offer hope.

“We’re mounting a reaction against the virus that is truly unprecedented,” said Dr. Melanie Ott, director of the Gladstone Institute of Virology in San Francisco.

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.

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.

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.

With so many proteins in its tool kit, the virus has many ways to counter our immune system; these also offer targets for potential vaccines and drugs. Researchers are working every angle. Most vaccine efforts are focused on disrupting the spike proteins, which allow entry into the cell. The drug remdesivir targets the virus’s replication machinery. Dr. Fehr studies how the virus disables our immune system.

For all the attention the virus has received, it is still new to science and rich in unknowns. “I’m still very focused on the question, How does the virus get into the body?” Dr. Ott said. “Which cells does it infect in the upper airway? How does it get into the lower airway, and from there to other organs? It’s absolutely not clear what the path is, or what the vulnerable path types are.

Even a photocopier is imperfect, and SARS-CoV-2 is no exception. When the virus commandeers a host cell to copy itself, invariably mistakes are made, an incorrect nucleotide swapped for the right one, for instance. In theory, such mutations, or an accumulation of them, could make a virus more infectious or deadly, or less so, but in the vast majority of cases, they do not affect a virus’s performance.

By March, at least 1,388 variants of the coronavirus had been detected around the world, all functionally identical as far as scientists could tell. Arrayed as an ancestral tree, these lineages reveal where and when the virus spread. For instance, the first confirmed case of Covid-19 in New York was announced on March 1, but an analysis of samples revealed that the virus had begun to circulate in the region weeks earlier. Unlike early cases on the West Coast, which were seeded by people arriving from China, these cases were seeded from Europe, and in turn seeded cases throughout much of the country.

The virus has no trouble finding us. But we are still struggling to find it; a recent model by epidemiologists at Columbia University estimated that for every documented infection in the United States, 12 more go undetected. Who has it, or had it, and who does not? A firm grasp of the virus’s whereabouts — using diagnostic tests, antibody tests and contact tracing — is essential to our bid to return normal life. But humanity’s immune response has been uneven.

“The best thing to come out of this pandemic is that everyone has become a virologist in some way,” Dr. Ott said. She has a regular trivia night with her family in Germany, over Zoom. Lately, the topic has centered on viruses, and she has been impressed by how much they know. “There’s so much more knowledge around,” she said. “A lot of wrong info around, also. But people have become so literate, because we all want it to go away.”

“For me right now, the place that I’m in, I really just most want to stop this virus,” she said. “It’s so frustrating and disappointing, to say the least, to be in this position in which we have stopped the world, in which we’ve created social distancing, in which we have created mass amounts of human devastation and collateral damage because we just weren’t prepared.

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