**4. Direct effects of SARS-CoV-2 in CNS**

There is evidence that SARS-CoV-2 can be present in CNS [17–19]. There are indications that SARS-CoV-2 can infect many CNS-resident cells [20, 21]. The presence of SARS-CoV-2 in cells is causing cellular dysfunction resulting in a variety of manifestations [22]. For example, infection of olfactory bulb neurons with SARS-CoV-2 will lead to olfactory dysfunction (dysosmia). In addition, infection of neurons involved in taste sensing will lead to the reduction of taste perception (ageusia). Dysosmia and ageusia have been observed early on in patients with COVID-19 [23]. Subsequently, evidence for direct infection of other parts of the CNS has been found (**Table 1**).

## **5. Vasculature and COVID-19**

SARS-CoV-2 infection can lead to endotheliitis [36, 40]. Endotheliitis, caused by SARS-CoV-2 infection also affect CNS vessels. In endotheliitis, there is an


#### *Neuroimmunology and Neurological Manifestations of COVID-19 DOI: http://dx.doi.org/10.5772/intechopen.103026*

*c, cerebral; C.e., clinical examination; CNS, central nervous system; CSF, cerebrospinal-fluid; CT, computer tomography; EEG, electroencephalography; NMR, nuclear magnetic resonance.*

#### **Table 1.**

*Manifestations of putative direct infection of cells with consequences in the CNS in COVID-19.*

accumulation of lymphocytes, neutrophils, and macrophages in endothelial walls. Endotheliitis can have major consequences eventually resulting in ischemic stroke. Also, alternative mechanisms of damage to large and small cerebral vessels by SARS-CoV-2 in COVID-19 have been observed [41]. In the heart, it has been shown that endotheliitis leads to small vessel vasculitis. This can also involve epicardial nerves in COVID-19 disease with the appearance of an inflammatory neuropathy, possibly resulting in cardiac complications such as myocardial injury and arrhythmias [42].
