The Prevalence of Coronavirus Infection and its Relationship with Lung Disease in Human beings

Abstract

The Corona Virus 2019 (COVID-19) is a highly contagious respiratory infection caused by the acute coronavirus syndrome (SARS-CoV-2). SARS-CoV-2 infects the alveolar epithelial cells (alveolar epithelial cells type 2 (AEC2)) through the angiotensin-converting enzyme receptor (ACE2). The occupancy of ACE2 by SARS-CoV-2, the increase of serum levels of free angiotensin II (Ang II) due to reducing ACE2-mediated degradation, activates the NF-kappa B path via the Ang II type 1 receptor (AT1R) and consequently leads to production of interleukin-6 (IL-6). SARS-CoV-2 also activates the innate immune system. The macrophage stimulation causes the overproduction of inflammatory cytokines, including IL-6, and the "cytokine storm," which leads to systemic inflammatory response syndrome and multiple organ failure. It seems that the combined effects of complement activation, irregular neutrophils, endothelial damage, and excessive coagulation is intertwined to stimulate the severe features of COVID-19.

Van der Made et al. (2020) reported 2 pairs of adult siblings from 2 unrelated families (family 1 Dutchman and family 2 African) suffering from severe respiratory failure associated with proven COVID19 infection (SARS-CoV-2)). Patients aged 21 to 32 years had no significant medical history, except for non-allergic rhinitis in one and a history of malaria infection in the other. None of them had a history of significant recurrent infections or chronic illness. Symptoms at the onset of the disease included cough, fever, shortness of breath, myalgia, and nausea with vomiting. The chest imaging showed bilateral pulmonary compositions or ground glass opacities with dense intrusions. It was variable all mechanical ventilation support required in the ICU; Time from onset of symptoms to admission to the ICU from 6 to 11 days and the time spent in the ICU from 10 to 16 days. One patient died at the age of 29 after developing a bacterial superinfection at the same time, while the others survived. One of the 3 survivors was readmitted due to right secondary pneumothorax. Laboratory studies have shown an appropriate increase in the number of white blood cells and an increase in the level of the inflammatory marker of C-reactive protein. Two tested patients had elevated D and ferritin dimers and one of them had fibrinogen.