Abstract
The human population is now faced to the pandemy of a new coronavirus SARS CoV-2. This highly pathogenic coronavirus entered to humans in late 2019 year probably transmitted from bats via still unknown animal vectors.
SARS CoV-2 is highly infectious with predominant respiratory route of transmission. Infected people are sources of infections even before the onset of clinical symptoms.
Whereas the natural course of SARS CoV-2 infection is indolent in large majority of infected people, there is the development of very severe inflammatory diseases in some patients, especially elderly and patients with various comorbidities. This could be explained by exagerated inflammatory response evoked by SARS CoV-2 in these predisposed patients.
Infected epithelial and endothelial cells are destroyed either by direct cytopatic effects of virus or by immune response. Damage associated molecular patterns which are released from dying cells are subsequently recognized by innate immunity cells via PRR receptors which are further fuelling adverse inflammation by production of proinflammatory cytokines and chemokines.
Special role is deserved to the abnormal cell death such as pyroptosis and neutrophils NETosis resulting in severe respiratory distress syndrome.