**2. Background**

SARS-CoV-2 is a beta-coronavirus [5]. The positive ssRNA genome encodes 16 nonstructural proteins involved in viral replication. Moreover, four structural proteins are for the envelope, spike-glycoprotein, the membrane, and the nucleocapsid [6]. Angiotensin-converting enzyme 2 (ACE2) is the receptor for uptake of SARS-CoV-2 [7–9]. Co-factors are heparan sulfates on the cell surface [10]. The spike protein is of major importance for interaction with ACE2 and cellular uptake. ACE2 is expressed in many cells of the body and therefore SARS-CoV-2 can infect most organs. SARS-CoV-2 uses the infected cell for the production of the virus. More receptors and host factors have been described for SARS-CoV-2 cellular entry [11, 12]. Most cells in the body express ACE2 receptors mediating SARS-CoV-2 uptake.

SARS-CoV-2 has the strongest effects on the lung [13, 14]. As a result of infection, SARS-CoV-2 leads to an atypical mainly interstitial pneumonia with patchy infiltrates. In severe cases, the lung can be completely affected resulting in loss of oxygenation. Besides the lung, any tissue can be infected by SARS-CoV-2 and damaged. As written further down and explained for the nervous system, the tissue damage can be a consequence of direct infection with the virus or indirect effects on the tissue due to a dysregulated immune response.
