Guest post by Ingrid R. Niesman, MS PhD
Recent headlines have many pet owners spooked, including myself. If there is one sure bet about viruses, they mutate and mutate rapidly. This epidemic is spreading extremely quickly and it was only a matter of time before a pet tested positive.
Let’s not equate dogs to cats
As of Friday, March 6, only two very weakly positive cases of Covid-19 have been found in pets, both in dogs. The bad news is that a 2008 publication in Vet Pathology has shown that disease in cats and ferrets infected with the related SARS-CoV virus resembles human SARS disease. Fortunately, ferret ownership is limited here in the US. However, cats in households are abundant. The good news is that, unlike dogs, indoor cats are unlikely to be exposed in the community, thus lessening the probability for infection.
What science tells us right now about cats and COVID-19
For clarity, SARS-CoV-2 is the actual virus name. COVID-19 is the disease. In a pace unheard of until now, scientists around the world are publishing information daily about the biology of the virus and the pathology of the disease. One of the first publications about how the virus infects humans used previous SARS studies to determine that this new novel virus uses a similar strategy to attach to cells and gain entry. ACE2, angiotensin-converting enzyme 2, is a surface protein highly expressed throughout the body, but has been recently found in concentrated pockets of specialized lung cells that aid in the reproduction of viral particles. Hence, this may be part of reason there is a predilection for the pneumonia that we see in many patients.
To quell my own curiosity about cats and Covid-19, I spent the morning aligning protein sequences. As a scientist, not a clinician, my first response is to look at the cell biology and protein structure. I first studied the brand-new structural models of SARS-CoV-2 binding to the ACE2 receptor (published March 4th in Science¹) showing which of the 805 amino acids of the human ACE2 interact with the sticky part of the virus. Several key areas are critical for this partnership to occur. When I aligned human, canine and feline amino acid sequences for ACE2 using freely available tools, I found no differences in the critical domains between human, cats and dogs. This is a problem. I was hoping to find that cats might have some differences that would make the ACE2-virus interaction less likely but clearly that is not the case.
So yes, we cannot totally rule out the possibility that cats are at risk for infection exists. But infection of cells doesn’t necessarily mean disseminated disease, and so far, no cat has tested positive. The only surefire way to determine the extent of potential cat disease is to intentionally infect cats, as was done in 2008, in a controlled experimental environment. Is this really necessary right now? Let’s concentrate on stopping the human spread instead.
The real danger lies when SARS-CoV-2 mutates. My main worry isn’t that my cats can become sick, but that somewhere out there two viruses are having a mixer of their own. This behavior is likely to happen in humans. As an example, the subtype II of Feline Infectious Peritonitis (FIP) is suspected to be a recombination with a similar canine virus. The best scenario is to keep this novel virus, which humans, dogs or cats, have probably never seen before, to a single species – humans – for now.
Keep your cats inside
The best advice is for us all is to remain vigilant in our communities, and to stay home if we are unwell, as has been the advice all along. If you keep your cats in a restricted environment and minimize contact with outside visitors, chances of infection will approach zero. Feral cats, by their nature, shun human contact and therefore are not at high risk for infection or transmission to humans. There is no need for large scale cullings to protect human populations.
Oh, and please don’t take your dog to the dog park if you are sick.
Ingrid R. Niesman MS PhD is the Director of the SDSU Electron Microscope Imaging Facility at San Diego State University. She graduated from Utah State University and received her MS from the University of Illinois-Urbana-Champaign. After 30 years of technical electron microscopy, cell biology, neuroscience and infectious disease research, Dr. Niesman completed her PhD in the UK at the University of Sunderland. Her work experience includes time at LSU Medical School, Washington University, UAMS in Little Rock, UCSD, TSRI and a postdoctoral year at CALIBR in La Jolla, CA. She has worked for at least two National Academy of Science members and is credited with over 50 publications. She can be reached at email@example.com
¹ ScienceMag.org, March 4, 2020 Structural basis for the recognition of the SARS-CoV-2 by full-length human ACE2