The neuroinvasive potential of SARS CoV2 may play a role in the respiratory failure of COVID 19 patients
Following the severe acute respiratory syndrome coronavirus (SARS CoV) and Middle East respiratory syndrome coronavirus (MERS CoV) another highly pathogenic coronavirus named SARS CoV 2 (previously known as 2019 nCoV) emerged in December 2019 in Wuhan, China, and rapidly spreads around the world. This virus shares highly homological sequence with SARS CoV, and causes acute, highly lethal pneumonia coronavirus disease 2019 (COVID 19) with clinical symptoms similar to those reported for SARS CoV and MERS CoV. The most characteristic symptom of patients with COVID 19 is respiratory distress, and most of the patients admitted to the intensive care could not breathe spontaneously. Additionally, some patients with COVID 19 also showed neurologic signs, such as headache, nausea, and vomiting. Increasing evidence shows that coronaviruses are not always confined to the respiratory tract and that they may also invade the central nervous system inducing neurological diseases. The infection of SARS CoV has been reported in the brains from both patients and experimental animals, where the brainstem was heavily infected. Furthermore, some coronaviruses have been demonstrated able to spread via a synapse connected route to the medullary cardiorespiratory center from the mechanoreceptors and chemoreceptors in the lung and lower respiratory airways. Considering the high similarity between SARS CoV and SARS CoV2, it remains to make clear whether the potential invasion of SARS CoV2 is partially responsible for the acute respiratory failure of patients with COVID 19. Awareness of this may have a guiding significance for the prevention and treatment of the SARS CoV 2 induced respiratory failure.
Journal of medical virology