Throughout the Covid-19 pandemic, sparse reports have been picked up of animals other than humans being affected by the disease. Domestic cats and dogs, as well as captive minks that have been culled for fear of spread and even a zoo’s tiger have tested positive, with each species exhibiting varying degrees of sickness. So, why is it that some animals get Covid while others don’t?
A new study published in the journal PLOS Computational Biology has narrowed down the cause using 3D protein modeling. Understanding why and how the disease passes between animals is a key discovery to control the spread as it helps us to see where it’s come from and where it could go.
SARS-CoV-2 likely initially came from bats, but where it went next is unclear as it’s suspected it went through an intermediary host before gracing our immune systems with its presence. Pangolins were highlighted as a potential culprit.
Since the virus went global, animals such as cattle and cats have been shown to be susceptible while pigs and chickens seem unaffected by the disease. To demystify the mystery, they looked at the cell surfaces of different animals to see how they interacted with SARS-CoV-2’s spike protein, which is known to bind to an ACE2 receptor protein on cell surfaces.
Using a computer to model different host-virus interactions, they were able to observe how well the spike protein was able to lock onto ACE2 inhibitors. It’s a bit like searching for the perfect lock to suit a key. Their results showed there were differences in how well the animals’ ACE2 “locks” fitted the SARS-CoV-2 key. Those whose ACE2 locks were the right fit correlated with the animals who have exhibited infection in real life.
While the simulations relied on approximations, they still carry water as they pinpointed features that were unique to the covid-susceptible ACE2 receptors. Therefore, if an animal's cells are lacking in these features, they are likely to be immune or experience less severe disease.
The researchers hope this information can contribute towards more effective antiviral treatments that could use artificial “locks” to bind with the virus before it has a chance to connect with an ACE2 receptor. It will also enable them to establish which species should be monitored for the disease so they can be treated or destroyed to prevent future outbreaks.
Study author João Rodrigues of Stanford University, California, said in a statement: “Thanks to open-access data, preprints, and freely available academic software, we went from wondering if tigers could catch Covid-19 to having 3D models of protein structures offering a possible explanation as to why that is the case in just a few weeks.”