A virus embedded in the Siberian permafrost was still infectious after 30,000 years, scientists reported in 2014. Meanwhile, the virus causing the COVID-19 disease only “survives” on surfaces hours or days, various virologists have been suggesting.
It has been demonstrated in the case of two other coronaviruses that made the leap from host animals to humans – the original SARS and MERS – that viral particles can remain active (be infectious) for up to about nine days. Not a year, let alone 30,000 of them.
The virus behind COVID-19, technically named SARS-CoV-2, has presumably been infecting its host animal, whatever it is, for eons. But it only came to the attention of science when it leaped to humans in 2019 and began to spread last December. That is why we don’t know much about SARS-CoV-2, let alone how long its stability is maintained out of the body, in aerosols or on surfaces.
The co-author of the original PNAS paper on the seemingly eternal virus, Prof. Emeritus Jean-Michel Claverie of the French National Research Center in Marseille, kindly explains how the one virus remained stable and infectious after 30,000 years, while the other becomes unstable and “dies” within hours to days.
Let us be clear that the virus that “came back to life” wasn’t a coronavirus or anything even remotely similar: It was a new species of DNA virus, which they named Pithovirus sibericum. The Pithovirus targets amoebas. In nature, SARS-CoV-2 is an RNA virus that probably targets an unidentified animal, possibly bats, pangolins or something else. But that isn’t the key difference.
It’s a cruel world outside
Viruses may have been the second form of life to evolve on the planet, after the earliest form of bacteria. Why the second, not the first? Because they are pure parasites. Viruses infect vulnerable cells onto which they can dock, injecting their DNA or RNA (depending on the viral species). That alien DNA or RNA enslaves the cells’ mechanisms to virtually cease doing what they normally do and produce viral progeny. The infected cell makes viruses until it bursts. So logically they couldn't have been first, they had to have something to host them.
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But outside the host, viruses are inert. They have no metabolism. They consist basically of an envelope of fats and/or proteins encasing the viral genetic code, DNA or RNA, and do nothing: they can’t eat or breathe or multiply. In fact, to this day there is a philosophical argument over whether they’re even a life-form or a biological chemical (“It’s a life-form,” a non-virologist once remarked. “It has an agenda”).
Anyway, unless a viral particle happens to fuse with a suitable cell, it can do nothing. And if they don’t infect a suitable cell within a short period of time, they “die” – meaning they lose their infectiousness. They may dock on a host cell and inject their genome, but enslavement will not ensue.
Why do coronaviruses in the outside world “die” within a day, a week, nine days or however long?
“Because our environment is remarkably hostile to microbes,” Claverie explains.
Live cells can repair damage to their DNA, for one thing. In the absence of any metabolism i.e., cellular activity, viruses can’t. In the outside world, the virus is exposed to air, specifically oxygen, which causes oxidation that damages DNA.
In another challenge to their viability, absent sufficient humidity virus particles become desiccated. At the other end of the fluid spectrum, liquid water may also disable them. And heat is not friendly to genetic material. So a virus on a shelf or a package or even a deodorant licked on a shelf store by a wannabe-influencer would not remain infectious for “long” (precise length to be determined). SARS and MERS can survive up to about nine days on steel and plastic, for instance, but there is no assurance that SARS-CoV-2 doesn’t survive longer. Or less.
Why would different viruses “survive” different lengths of time on a given surface?
The difference probably lies in the composition of the particle’s “wall,” Claverie says. Some viral envelopes are more robust than others: “The coronavirus is enveloped by a layer of lipid (a fat like oil or butter), and this layer must be intact to infect cells by fusion of this virus’ membrane with that of the cell. No membrane around, no fusion, no infection,” he explains.
Lipid-enveloped viruses are more vulnerable than non-enveloped ones (with an external layer of proteins), which can be very tough. The Pithovirus that could still infect its victims after 30,000 years had a tough protein envelope, Claverie clarifies.
But chiefly, it was protected from the environment. The Pithovirus had been buried in permafrost: it was cold, there was no oxygen, no light, and no liquid water. “Permafrost is ideal to keep the virus particle intact,” he explains.
So, a lipid-encased coronavirus particle contaminating a box of tissues in Florida or London isn’t likely to remain infectious after 30,000 years.
How long the newly discovered coronavirus remains infectious on nonbiological surfaces is being investigated. Claverie shares his opinion that suggestions of its virility for hours to days on different surfaces may be overestimated.
“In the lab, if you start from millions of particles, and wait, even if a single one remain intact, you may be able to ‘restart’ an infection on cell culture ‘in vitro,’” he tells Haaretz. “In the real world, you need to be in contact with many particles at once (sometimes thousands) to get an infection, so the in vitro numbers do not apply. Washing your hands after using the cart at the supermarket is a good thing to do.”
If the ancient virus was still infectious after thawing 30,000 years after it last infected an amoeba, does it imply that coronaviruses trapped in frozen sputum in our freezer might still be infectious for years? Even 30,000 years, assuming the Israel Electric Company and the freezer motor last that long?
“Spitting in your fridge is not a good idea, since this is the way most viruses are kept in the labs,” Claverie advises.
However, not all viruses are the same. The Pithovirus loved being frozen. But some viral species don’t like it at all and do not “restart,” he observes. “For them to ‘survive’ freezing requires specific solvents (like glycerol) that preclude the formation of micro-crystals of ice which disrupt their structure. But yes: some viruses can be still infectious after years in the freezer (like the smallpox virus).”
On the hopeful side: the coronavirus is a lipid-enveloped virus, which is more fragile than protein-enveloped viruses. Also, in your freezer, in contrast to the Siberian permafrost, you still have oxidation going on. In addition: “Coronaviruses, like many pathogenic viruses for humans, have genomes made of RNA, not DNA (like smallpox and our prehistoric viruses),” Claverie says. “RNA is a much more fragile chemical compound than DNA. One more [piece of] good news.”
We will just add that the Pithovirus revived by thawing after 30,000 years was a giant DNA virus – so huge that it can be seen through an ordinary light microscope, about 500 nanometers in diameter. SARS-CoV-2 virions are about 50 to 200 nanometers in diameter. You can't see them through an ordinary microscope.
It isn’t only viruses that attack amoebas coming out of the thawing permafrost, though. In 2016, during unusually hot weather, thousands of reindeer and 72 people in the Yamal Peninsula, Siberia, contracted anthrax. Russian scientists believe the bacteria originated in bacterial spores liberated from thawing permafrost, maybe from a long-dead reindeer.
As Claverie and the team at the time summed up in their 2014 paper: The revival of such ancestral amoeba-infecting viruses suggests that the thawing of permafrost – as is happening apace thanks to global warming – could spring additional microbial surprises. “Microorganisms living on and within the early humans who populated the Arctic could still be frozen in the soil,” Claverie told Scientific American in 2016. We know Neanderthals and Denisovans both lived in Siberia, and we may yet get to meet if not them, then the germs that infected them.