乌鸦传媒

In this video, Benjamin tenOever, PhD, of NYU Langone Health's Departments of Microbiology and Medicine in New York City, discusses the recent concerns in Hong Kong about hamsters spreading new COVID-19 strains and whether we need to be concerned about our own pets putting us in danger.

The following is a transcript of his remarks:

An answer to that question of whether or not the emergence of Omicron in China was a direct result of hamster imports is an impossible question to ever answer. But it is true that it is in the realm of possibility.

You know, we as a research community have been using hamsters to study the biology of SARS-CoV-2, which is obviously the underlying virus that causes COVID. And hamsters have been the primary small animal model to study the disease because of the receptor called ACE2 that allows the virus to get into cells.

The hamster happens to encode an ACE2 that looks a lot like the human ACE2, and so the virus essentially chose the ability to infect hamsters by its evolution. So even though we most often use mice or rats for our small animal models, hamsters have always been incredibly susceptible to all the variants and they show disease that very much looks like COVID-19 in humans.

You know, I have two little girls at home and they have friends that have hamsters, and I have warned their parents. Not that I'm worried that the hamsters are going to contribute to any new dynamics in the pandemic, but more than that, should they get a SARS-CoV-2 infection, if they give it to their hamsters, there's a good possibility that their hamsters will die.

The truth is that you are more of a threat to them than they are a threat to the pandemic.

All vertebrates have some version of ACE2 in their bodies. You can look at all of the ACE2 sequences in all of the vertebrate species and with pretty good accuracy determine which ones would be susceptible to virus and which ones would not be. All of these animals, which exist in the wild as well, could certainly contract the disease and it could then evolve in that population.

Now, the question of whether or not we should be concerned about it coming back and infecting us, like the situation in Hong Kong, where they're concerned about pets -- that's a more real possibility in that people do socialize in very close contact with their pets.

And so the chances that you could give a virus to your pet or the pet could give a virus to you, of course, is much higher the closer you interact with these animals. Whereas like a deer in the wild, you know, if a virus is evolving there it's not necessarily a foregone conclusion that it will come back into humans.

The real aspect here that is important to remember is that while ACE2 is certainly a critical factor that allows the virus to enter into an individual, that's not the whole story. Obviously we have evolved to have very sophisticated defenses against these viruses, and so the ability of the virus to infect a cell is one thing, but the ability of that virus to cause disease is an entirely separate category.

In that category, every vertebrate species is also going to have different versions of those defenses. It's the same principle, but the proteins that encode them are a little bit different. Which means that the -- we call them "antagonistic strategies" -- the virus that makes SARS-CoV-2 makes probably about half a dozen proteins that are designed not for replication of the virus, but are designed strictly to inhibit different aspects of our immune defenses.

That's essentially why we get COVID-19 -- because our defenses are ineffective at clearing the virus, which is the difference between, you know, getting sick asymptomatically or getting a stuffy nose versus actually getting hospitalized and having difficulty breathing.

So even if, you know, SARS-CoV-2 were to jump into another species, evolve in that species, mutate in that species, and then be re-introduced back into the human population, the scary part is that that provides a lot of time for the virus to evolve and change, which could be bad. But in general that usually causes the virus to actually weaken, because the virus will adapt to that new species, and adaptation to that new species will often compromise some of those antagonistic strategies that the virus has that cause us disease.

If Omicron came from deer or narwhal or mice or hamsters or whatever animal in the wild, I would expect to see mutations outside of spike. So you would see mutations in spike, but maybe you would also see mutations in the nuclear protein, which is involved in antagonism, or a protein called ORF6b, which is involved in antagonism, or in the protease, which is involved in antagonism. But none of these proteins have any changes in them at all, which would probably be necessary should the virus have been forced to adapt to a new defense system.

And so that's also why BA.2, which is the next lineage of Omicron, is a little bit more noteworthy in that BA.2 does have some mutations in this very large, we call it a polyprotein that makes many proteins, called ORF1ab, and that one does have some reports of it being involved in antagonizing the defenses.

And so for the first time, we see maybe some evidence of a strain that went into one species and came out with a few new mutations that aren't in just the spike protein. But again, there aren't very many of them, and I would expect it to be, if anything, more attenuated, meaning more weakened, when it came back into the human population for that reason.

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