Covid-19 | The coronavirus isn’t alive. That’s why it’s so hard to kill.

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The coronavirus isn’t alive. That’s why it’s so hard to kill.

Viruses have spent billions of years perfecting the art of surviving without living — a frighteningly effective strategy that makes them a potent threat in today’s world.

That’s especially true of the deadly new coronavirus that has brought global society to a screeching halt. It’s little more than a packet of genetic material surrounded by a spiky protein shell one-thousandth the width of an eyelash, and leads such a zombielike existence that it’s barely considered a living organism.

But as soon as it gets into a human airway, the virus hijacks our cells to create millions more versions of itself.

There is a certain evil genius to how this coronavirus pathogen works: It finds easy purchase in humans without them knowing. Before its first host even develops symptoms, it is already spreading its replicas everywhere, moving onto its next victim. It is powerfully deadly in some but mild enough in others to escape containment. And, for now, we have no way of stopping it.

As researchers race to develop drugs and vaccines for the disease that has already sickened 350,000 and killed more than 15,000 people, and counting, this is a scientific portrait of what they are up against. 

‘Between chemistry and biology’

Respiratory viruses tend to infect and replicate in two places: In the nose and throat, where they are highly contagious, or lower in the lungs, where they spread less easily but are much more deadly.

This new coronavirus, SARS-CoV-2, adeptly cuts the difference. It dwells in the upper respiratory tract, where it is easily sneezed or coughed onto its next victim. But in some patients, it can lodge itself deep within the lungs, where the disease can kill. That combination gives it the contagiousness of some colds, along with some of the lethality of its close molecular cousin SARS, which caused a 2002-2003 outbreak in Asia.

Another insidious characteristic of this virus: By giving up that bit of lethality, its symptoms emerge less readily than SARS, which means people often pass it to others before they even know they have it.

It is, in other words, just sneaky enough to wreak worldwide havoc.

Viruses much like this one have been responsible for many of the most destructive outbreaks of the past 100 years: the flus of 1918, 1957 and 1968; and SARS, MERS and Ebola. Like the coronavirus, all these diseases are zoonotic — they jumped from an animal population into humans. And all are caused by viruses that encode their genetic material in RNA. 

That’s no coincidence, scientists say. The zombielike existence of RNA viruses makes them easy to catch and hard to kill. 

Outside a host, viruses are dormant. They have none of the traditional trappings of life: metabolism, motion, the ability to reproduce.

And they can last this way for quite a long time. Recent laboratory research showed that, although SARS-CoV-2 typically degrades in minutes or a few hours outside a host, some particles can remain viable — potentially infectious — on cardboard for up to 24 hours and on plastic and stainless steel for up to three days. In 2014, a virus frozen in permafrost for 30,000 years that scientists retrieved was able to infect an amoeba after being revived in the lab.

When viruses encounter a host, they use proteins on their surfaces to unlock and invade its unsuspecting cells. Then they take control of those cells’ own molecular machinery to produce and assemble the materials needed for more viruses.

“It’s switching between alive and not alive,” said Gary Whittaker, a Cornell University professor of virology. He described a virus as being somewhere “between chemistry and biology.”
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