A consideration of publication-derived immune-related associations in Coronavirus and related lung damaging diseases

Nophar Geifman; Anthony D Whetton

The recent respiratory disease pandemic [1] , caused by the severe acute respiratory syndrome (SARS) coronavirus 2 (SARS-CoV-2), has both high rates of infection as well as high mortality rates [2, 3] . In many inflammatory diseases, signaling proteins termed cytokines play a critical role in disease pathology. These proteins are secreted mainly from hematopoietic cells including lymphocytes and macrophages, and along with such cells, play a central role in many diseases as well as in health [4] [5] [6] [7] . In the case of COVID-19, and other viral diseases, they can significantly affect the course and outcome for the patient. This may manifest itself as a cytokine release syndrome or cytokine storm, observed in many patients as highly elevated levels of these proteins during acute disease. While first linked to the 1918 influenza pandemic [8] the cytokine storm was extensively documented in the avian H5N1 influenza virus infection [9] . H5N1 influenza virus causes acute lung injury as also observed in COVID-19. Acute respiratory distress syndrome (ARDS) is the principal cause of respiratory failure associated with severe influenza as it is with COVID-19 and other members of the Coronavirus family. In severe influenza infections the extent of lung injury is due to dysregulated inflammatory responses. Hence, to compare and contrast immune-related trends in H5N1 influenza and coronavirus infections could enable clinical research to more effectively consider treatment options.