The Pathophysiology of COVID-19

Abstract

Background: On Dec 19, 2019, the public health department of China reported that an outbreak of pneumonia was caused by a novel Coronavirus. On March 11, 2020, the World Health Department (WHO) declared a worldwide pandemic. Understanding the pathophysiology of the SARS-COV-2 virus is necessary for understanding the transmission, clinical presentation, associated risk factors, predicted outcomes, and provides guidance for treatment protocols.

Methodology: A comprehensive PubMed search was performed utilizing the terms: COVID-19 in combination with the terms virulence (507), and/or
pathophysiology (490) leading to 997 results. These results were then screened for relevance. Categorized, and evaluated under the auspices of making good pathophysiological sense.

Results: The SARS-COV-2 virus is much more virulent than either the SAR’s or MER’s virus with its ability to cause serious disease inversely dependent
on a person’s ability to produce T-cells. The ability to produce T-cells declines linearly until the age of 65. The ACE-2 receptor binding site does not vary among different ethnic groups, but initial evidence suggests there may be differences ACE-2 expression levels. This variance in expression level may explain different infectivity rates but not clinical outcome. The clinical outcome seems more related to the cytokine storm. Obesity, asthma, and COPD may decrease one’s likelihood of being infected but increases the morbidity rates once infected along with poor diet, hypertension, diabetes, and immunodeficiency.

Conclusions: The underlying pathophysiology of COVID-19 explains not only the virulence, and clinical presentation, and suggest adverse clinical responses are related to dysregulation of the immune response.