ACE2 Structural Model Used to Predict Species Susceptibility to SARS-CoV-2

Numerous animals may be vulnerable to SARS-CoV-2, according to a large study modelling how the virus might infect different animals' cells. The study, published today in Scientific Reports, suggests that 26 animals regularly in contact with people may be susceptible to infection.

The focus of the investigation was whether mutations in the ACE2 protein in 215 different animals, that make it different from the human version, would reduce the stability of the binding complex between the virus protein and host protein.

The researchers found that for some animals, such as sheep and great apes, the proteins would be able to bind together just as strongly as they do when the virus infects people. Some of the animals, such as sheep, have not yet been studied with infection tests, so this does not confirm that the animal can indeed be infected.

Lead author Professor Christine Orengo, from University College London, said: "We wanted to look beyond just the animals that had been studied experimentally, to see which animals might be at risk of infection, and would warrant further investigation and possible monitoring.

"The animals we identified may be at risk of outbreaks that could threaten endangered species or harm the livelihoods of farmers. The animals might also act as reservoirs of the virus, with the potential to re-infect humans later on, as has been documented on mink farms."

The research team also performed more detailed structural analyses for certain animals, to gain a better understanding of how infection risks may differ across animal species. By comparing their findings to other experimental data, they set thresholds to predict which animals are at risk of infection, and which ones most likely cannot be infected.

They found that most birds, fish, and reptiles do not appear to be at risk of infection, but the majority of the mammals they reviewed could potentially be infected.

Professor Orengo added: "The details of host infection and severity of response are more complex than just the interactions of the spike protein with ACE2, so our research is continuing to explore interactions involving other host virus proteins."