Li, Yan‐Chao, et al. “The Neuroinvasive Potential of SARS‐CoV2 May Play a Role in the Respiratory Failure of COVID‐19 Patients.” Journal of Medical Virology, vol. 92, no. 6, 2020, pp. 552–555., doi:10.1002/jmv.25728.

https://onlinelibrary.wiley.com/doi/full/10.1002/jmv.25728

Smith College

SARS-CoV and MERS-CoV, two other betacoronaviruses, bear a striking resemblance to SARS-CoV-2, therefore studies done on neural infection in these alternate betacoronaviruses may help us glean insight on the neuroinvasive potential of SARS-CoV-2. Even though the expression level of ACE2 receptors (likely responsible for mediating the entry of both SARS-CoV and SARS-CoV-2) in the CNS is very low under normal conditions, SARS-CoV has been found in the neurons of the CNS. It is unclear exactly how betcoronaviruses can enter the neurons in CNS, but some hypotheses include entry via either the hematogenous or lymphatic route or via the PNS. Another betacoronavirus, avian bronchitis virus, infects the brainstem. The areas of the brainstem that it infects includes the solitary tract, which receives sensory input from the lungs and respiratory tract, and the nucleus ambiguus, which, along with the solitary tract, innervates airways smooth muscle, gland, and blood vessels. Infection in these areas that serve the overall purpose of the cardiorespiratory centre in the brainstem is the typical cause of death in infected animals. Our knowledge about SARS-CoV-2 can be expanded by understanding other betacoronaviruses, especially SARS-CoV and MERS-CoV.

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