These observations were thought to be due to ACE2 expression on neurons and glial cells of the brain (41) allowing the virus to directly reach the brain via the olfactory bulb following inhalation without the use of ACE2, however, this was strongly refuted by growing evidence that support these neurological findings are mainly attributed to the effects of hypoxia, coagulopathy, and multi-organ damage in severe infection, accompanied by virus-mediated inflammatory processes (74). Here, ACE2 is linked to infection.