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Aim: The infection of the nasal mucosa and the lungs by CoV-2 may spread to the CNS, including the brainstem, thereby playing a potential key role in the severe respiratory distress observed in COVID-19. Although several clinical observations support this hypothesis, the knowledge in this field is very limited. To fill this gap, we will investigate CoV-2 neuroinvasion in humans, animal models, and cell culture-based experimental models and decipher the molecular mechanisms involved. Results of this project will provide clues on whether targeting potential neurotropism of CoV-2 may be relevant approach for experimental therapeutics in Covid-19.