Let’s just call this an “odds and ends” post. I’ll outline some interesting highlights from some recent papers, including a couple just posted overnight.
This study looked at genomic data from 410 vertebrates, including 252 mammals, and the researchers ranked the different animal species in terms of their predicted susceptibility to SARS-COV-2. This isn’t particularly new, as the first paper looking at the virus’ receptor (ACE2) in different animal species was published a couple of months ago, but this was a larger study that took a much broader approach. Here are some noteworthy results:
- The very high risk category included people (duh), gorillas, orangutans and various other non-human primates
- The high risk category included a wide array of species, including critters such as the Chinese hamster, Narrow-ridged finless porpoise, white tailed deer, giant anteater, orca and reindeer.
- Cats fell into the medium risk group, a bit surprising since we know from experimental and limited field evidence that cats are susceptible to infection.
- Dogs were low risk, which fits with what we know from other work.
- Ferrets were ranked very low risk, which is contrary to experimental studies done to date. The authors suggested that maybe the virus uses a different receptor in ferrets. That would be surprising though. The result maybe just indicates how “predicted” and “real life” don’t always line up.
This paper looked at transmission of SARS-CoV-2 between ferrets. They infected four ferrets, then 6 hours later added uninfected ferrets to the same cages, and to adjacent cages that were separated by steel grids, 10 cm apart.
Virus levels in respiratory secretions peaked 3 days after infection, and were detectable for 11 days in two ferrets, and for 15 days and 19 days respectively in two others (that’s pretty long).
All 4 ferrets added to the cages became infected, while 3 of the 4 ferrets in adjacent cages became infected.
This doesn’t add a lot of new information to previous ferret studies, but provides more evidence that ferrets are susceptible (despite the predictions from the study above) , that they can shed the virus for a relatively long time, and that they can infect other ferrets. Since they can infect other ferrets in adjacent cages, we have to assume there’s some risk that an infected ferret could transmit the virus to a person if they had close contact. This just re-inforces our standard messages about staying away from pets when you’re sick, and if COVID-19 is present in a household, pets should be kept inside and away from others.
There’s been some stir about the potential for the anti-parasitic medication ivermectin to treat COVID-19 in people, based on an in vitro study and some weak anecdotes. That hasn’t stopped people asking vets for more heartworm medication “for their dog” in the meantime. The potential for ivermectin to be of any significant benefit in treating SARS-CoV-2 infection hasn’t seemed very strong, and this pharmacokinetic study supports that skepticism.
The overall message from this paper is that the levels of ivermectin that you can get in the body are “are orders of magnitude lower, as compared to the in vitro antiviral end-points, described in the study of Caly et al.” The 5 umol/L level of ivermectin that effectively eliminated almost all the virus in vitro is more than 50 times higher than what you get in the body even with a higher dose of ivermectin (i.e. 700 ug/kg) than what is normally used (i.e. 150-200 ug/kg).
So, although ivermectin can kill SARS-CoV-2, it takes a lot more than you would get with normal dosing. Trying to increase the dose to get levels that would kill the virus might be more likely to kill the patient from drug toxicity. The authors’ well-said conclusion was “…the experimental design is based on clinically irrelevant drug levels with inhibitory concentrations whose targeting in a clinical trial seems doubtful at best.”