To witness a dog come down with Covid-19 is a curious thing. Though mine have been spared, I have a friend whose two dogs got sick in addition to the rest of their family. In videos my friend sent me, I could see the dogs were lethargic, sneezy, and seemingly suffering. While most of the domestic pets that tested positive for the disease last year didn’t exhibit symptoms like theirs, those that did mirrored the mild infections we experience as humans, tiring easily and developing colds.
The good news is that my friend’s dogs made a smooth recovery. (So did their family members.) The not-so-good news is that new variants of SARS-CoV-2, which we now know are more infectious and more dangerous than the original strain, might have adapted to animals as well as they’ve adapted to us—our favorite household pets included. While the original strain was already capable of infecting enough animal species to fill Noah’s ark—among them minks, ferrets, weasels, dogs, lions, tigers, and cats, oh my—the new variants are even more adventurous, finding a home in an even larger range of animal hosts. According to new studies, the animals that were vulnerable to the original strain may also be at greater risk of getting sick from the new variants.
The first variant to garner global attention was B.1.1.7, also known as the UK variant. At least 50 percent more transmissible than the previously dominant SARS-CoV-2 strain, B.1.1.7 likely contributed to the surge in new Covid-19 cases that swept through Britain in late December and early January and is now wreaking havoc across Europe and expanding rapidly in the United States. No coincidence is it, then, that the location of the first study I’ll discuss, a preprint still undergoing peer review but available to read on bioRxiv, was a veterinary center outside London.
From December to February—precisely the same timeframe that B.1.1.7 had its catastrophic rise and fall—the Ralph Veterinary Referral Centre noticed a significant uptick in the number of pets, in particular cats and dogs, admitted to its cardiology unit with myocarditis, an inflammatory condition of the heart that at its worst can lead to heart failure. In just two months, incidence of myocarditis increased ninefold, from 1.4 to 12.8 percent. The study focuses on eight cats and three dogs who were treated for myocarditis at the center. Their owners reported similar symptoms—acute lethargy, loss of appetite, fainting. Further cardiac testing revealed that the pets had excess fluid in their lungs and arrhythmic heartbeats. All 11 had one thing in common: they were exhibiting telltale signs of Covid-19.
Prior to taking their pets to the vet, five of the pet owners had already been diagnosed with Covid-19. Ultimately six of the 11 pets—four cats and two dogs—tested positive, either through PCR or antibody diagnostics, for SARS-CoV-2. The three diagnosed via PCR had the B.1.1.7 variant—the first pets on record to be infected with the ultra-contagious strain. They wouldn’t be the last. In mid-March, researchers across the pond at Texas A&M University announced that a dog and cat from the same home in Brazos County, Texas tested positive for the B.1.1.7 variant. Though all of the pets, with the exception of one cat that relapsed and was later euthanized, are now in good health, it isn’t a good sign that B.1.1.7 seemed to take a greater toll on the pets it infected than what was observed with the original strain.
More severe symptoms isn’t the only cause for concern, however. There is also the issue of a more expansive host range—meaning the new variants might be spreading among animal populations it couldn’t reach before. Common breeds of laboratory mice were once included in this out-of-range species pool, due to the fact that the original SARS-CoV-2 strain couldn’t bind as well to the mouse ACE-2 receptors as it could to those in humans. But according to another recent preprint, this is no longer the case.
The French researchers who conducted the study injected 8-week-old mice with either the original strain or one of the most common new variants—B.1.1.7, B.1.351, or P.1. The original strain, as expected, was unable to take hold and start replicating in the mice inoculated with it. The new variants, by contrast, not only replicated quite efficiently in mice airways, but reached high titers as well, with B.1.351 and P.1 yielding the highest. This finding is consistent with previous studies in humans, which establish a consistent link between the mutations exhibited by B.1.351 and P.1 and a greater potential for infectivity and immune escape.
Though none of the mice developed symptoms, whether or not more mice are getting sick isn’t exactly the worst of our problems. Far more concerning is the possibility that this virus is circulating among mice and evolving fitter, more virulent versions of itself. Rodents, the French researchers pointed out, “have been hypothesized as the ancestral host of some betacoronaviruses.” And who doesn’t have mousetraps in their apartment or basement? Were mice to become yet another animal reservoir for SARS-CoV-2 to incubate in, the potential for cross-species transmission would be alarmingly high. Such patterns in viral variation and transmission have already been noted and studied in Danish mink farms, where virus originated with farmhands, ripped through the closely packed minks, and jumped back full circle, slightly varied, into human handlers.
Even if public health measures and medical interventions succeed in eliminating Covid-19 from humans, there is still the entire living ecosystem to consider. This disease has reached 125 million humans so far, and that’s only the cases we’ve officially confirmed. It would be naive to assume that the ripple effects of numbers this large haven’t penetrated deep into the rest of the biosphere, especially when we consider that many animals, like mice and like us, have ACE-2 receptors ripe for the taking. Across 130 species of mammals, 75 species of birds, 67 species of bone fish, and several more, a group of scientists has identified 80 ACE-2 proteins that could potentially facilitate binding to SARS-CoV-2. But identification is only the first step of many we must take to prevent another lethal leap from an animal reservoir to humans.
More animal reservoirs means more opportunities for SARS-CoV-2 and other coronaviruses to hide in plain sight, where they can comfortably evolve and become more dangerous without human interference. We need a comprehensive, integrated, and adaptive surveillance framework that can rapidly detect any emergent coronaviruses in suspect populations. Just as important is the development of pipelines for altering coronavirus vaccines and drugs that their makers can turn to if their previous technologies fail to neutralize a new variant. The next animal to bring a deadly virus to our doorstep needn’t be an exotic bat. It could be a cat, a dog, or the lowly field mouse that makes its nest in your home every winter.