From Cats And Canines To Minks And Mice, Covid-19 Variants Are Infecting The Ecosystem

A photo of the author’s dog, Sky.

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Watching a dog come down with Covid-19 is a strange thing. Although mine were spared, I have a friend whose two dogs, along with the rest of their family, got sick. I could see in videos my friend sent me that the dogs were sluggish, sneezing, and seemingly suffering. While most pets that tested positive for the disease last year didn’t show symptoms like theirs, those that reflected the mild infections we experience as humans are easily tired and develop colds.

The good news is my friend’s dogs made a smooth recovery. (Your family members too.) The not-so-good news is that new varieties of SARS-CoV-2, which we now know are more contagious and dangerous than the original strain, may adapt to both animals and animals I’ve adapted to us – our favorite pets included. While the original tribe was already able to infect enough animal species to fill Noah’s ark – including minks, ferrets, weasels, dogs, lions, tigers, and cats, oh my god – the new variants are even more adventurous and are finding one At home in an even wider range of pet owners. Recent studies have shown that animals that were susceptible to the original strain may also be at higher risk of developing the new variants.

The first variant that attracted worldwide attention was B.1.1.7, also known as the UK variant. B.1.1.7 is at least 50 percent more transmissible than the previously dominant SARS-CoV-2 strain and has likely contributed to the surge in new Covid-19 cases that swept the UK in late December and early January and are now chaos across Europe wreak havoc and expand rapidly in the United States. So it is no coincidence that the location of the first study I’ll discuss, a preprint that is still peer reviewed but can be read on bioRxiv, was a veterinary center outside of London.

From December to February – the very same period that B.1.1.7 experienced a catastrophic rise and fall – the Ralph Veterinary Referral Center noted a significant increase in the number of pets, particularly cats and dogs, with myocarditis in its Cardiology, an inflammatory disease of the heart that, in the worst case scenario, can lead to heart failure. In just two months, the incidence of myocarditis increased nine-fold from 1.4 to 12.8 percent. The study focuses on eight cats and three dogs treated for myocarditis at the center. Their owners reported similar symptoms – acute lethargy, loss of appetite, fainting. Additional heart tests revealed that the pets had excess fluid in their lungs and abnormal heart rhythms. All 11 had one thing in common: they showed tell-tale signs of Covid-19.

Before they took their pets to the vet, five pet owners were diagnosed with Covid-19. Ultimately, six of the eleven pets – four cats and two dogs – tested positive for SARS-CoV-2 either by PCR or antibody diagnostics. The three diagnosed using PCR had variant B.1.1.7 – the first registered pets infected with the ultra-contagious strain. You 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 variant B.1.1.7. While all pets are now in good health except for one cat who relapsed and was later euthanized, this is not a good sign that B.1.1.7 appeared to stress the infected pets more than what was with the original strain was observed.

However, more severe symptoms are not just a cause for concern. There is also the problem of a more expansive host range – which means that the new variants may spread to animal populations that could not previously be reached. Common breeds of laboratory mice were once included in this out-of-range species pool because the original SARS-CoV-2 strain could not bind to ACE-2 receptors in mice as well as they did in humans. However, according to another current 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. As expected, the original strain was unable to multiply and replicate in the mice inoculated with it. In contrast, the new variants not only replicated very efficiently in the airways of mice, but also achieved high titers, with B.1.351 and P.1 giving the highest results. This finding is in line with previous studies in humans, which establish a consistent association between the mutations shown by B.1.351 and P.1 and a greater potential for infectivity and immune escape.

While none of the mice developed symptoms, whether or not more mice get sick isn’t our worst problem. Far more worrying is the possibility that this virus will circulate among mice and become fitter and more virulent. The French researchers indicated that rodents “have been adopted as the primary hosts of some beta coronaviruses”. And who doesn’t have mousetraps in their apartment or in the basement? If mice were to become another animal reservoir for the incubation of SARS-CoV-2, the potential for cross-species transmission would be alarmingly high. Such patterns of virus variation and transmission have already been identified and studied in Danish mink farms, where viruses originated from farm workers, tore through the tightly packed minks and, slightly varied, the circle jumped back into human handlers.

Even if public health measures and medical interventions succeed in removing Covid-19 from humans, the entire living ecosystem still needs to be taken into account. This disease has reached 125 million people so far and these are just the cases that we have officially confirmed. It would be naive to assume that the ripple effects of such large numbers did not penetrate deep into the rest of the biosphere, especially considering that many animals, like mice and like us, have ACE-2 receptors that are ripe for ingestion . In 130 species of mammals, 75 species of birds, 67 species of bony fish, and several other species, a group of scientists has identified 80 ACE-2 proteins that could potentially facilitate binding to SARS-CoV-2. However, identification is just the first of many steps we must take to prevent another fatal leap from animal reservoirs to humans.

More animal reservoirs mean more opportunities for SARS-CoV-2 and other coronaviruses to hide in sight, where they can develop comfortably and become more dangerous without human intervention. We need a comprehensive, integrated and adaptable surveillance framework that can quickly detect coronaviruses in suspicious populations. Equally important is the development of pipelines to modify coronavirus vaccines and drugs that their manufacturers can turn to if their previous technologies fail to neutralize a new variant. The next animal to bring a deadly virus to our doorstep doesn’t have to be an exotic bat. It could be a cat, dog, or the low-field mouse that builds its nest in your home every winter.

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