*1.1. Pathophysiology in Coronaviral Infections*

All coronaviruses have a different antigenicity, depending on the spike (S-) protein of the virus. In contrast to influenza viruses, the S-proteins in coronaviruses are very stable. To enter the human cell, coronaviruses use different human cell surface peptidases. Both SARS-CoV and SARS-CoV-2 use the human angiotensin-converting enzyme-2 (ACE-2), which functions as a receptor for the virus. This receptor is widely expressed in a number of organs including pulmonary tissue, as well as in monocytes and macrophages [3]. Recent studies also demonstrated that both SARS-CoV and SARS-CoV-2 also can use lectins to enter the cell. Moreover, SARS-CoV-2 can use neuropilin-1, which is strongly expressed by endothelial cells and epithelial cells facing the nasal cavity [4–6].

Entering the cytoplasm by the receptor, the virus uncoats and starts replicating in the human cell. The exact pathophysiology responsible for the unusually high morbidity and mortality following CoV infections with high pathogenicity, are incompletely understood. Important mechanisms could be the virus-induced direct cytopathic effects, as well as the viral evasion of the host immune system.
