Table 1.
Comparison between corona virus-related illnesses those posed significant public health issues
| Characteristics | MERS | SARS | COVID-19 |
|---|---|---|---|
| Status | First reported in Saudi Arabia in September 2012, 27 countries affected, 2519 people infected, 866 deaths | First reported in Asia in February 2003, 26 countries affected, 8000 people infected, 774 deaths | First reported in Wuhan, China in December 2019, causative agent identified in January 2020. 4,525,497 as of 17th May, 2020, with 307,395 deaths and a total of 215 countries/geographic location |
| Causative virus | MERS-CoV | SARS-CoV | SARS-CoV-2 |
| Tissue tropism | Pneumocytes, pulmonary macrophages, macrophages infiltrating the skeletal muscles, and renal proximal tubular epithelial cells | Pneumocytes, lymphocytes, monocytes, and lymphoid tissues, intestinal mucosa, renal distal tubular epithelial cells, neurons in the brain, and tissue-resident macrophages in different organs | Pneumocytes, intestinal mucosa, renal distal tubular epithelial cells, and endothelium |
| Clinical Features | Severe acute respiratory illness, including fever, cough, and shortness of breath | Flu-like illness, including fever, chills, cough, and malaise. 70% of the patients subsequently suffer from shortness of breath and recurrent or persistent fever, and 30% show clinical improvement after the first week | Fever, dry cough, fatigue, shortness of breath, bone pain, and sore throat as well as a rather specific smell- and taste sensational loss. Some patients present with gastrointestinal symptoms such as nausea, vomiting, and diarrhea. Some patients have a relatively stable clinical course for 5 to 8 days followed by acute and very rapid deterioration in patients, who may run into a critical course afterwards. Advanced cases generally had respiratory, cardiovascular, and renal failure. |
| Macroscopy/Gross | Edematous lungs with increased gross weight and multiple areas of congestion | Edematous lungs with increased gross weight and multiple areas of congestion, enlargement of lymph nodes in the pulmonary hila and the abdominal cavity, diminished spleen size, and weight | Edematous lungs with increased gross weights, multiple areas of congestion, and pulmonary embolism |
| Microscopya | Exudative diffuse alveolar damage with hyaline membranes, pulmonary edema, type II pneumocyte hyperplasia, interstitial lymphocytosis, multinucleate syncytial cells, bronchial submucosal gland necrosis, acute tubulointerstitial nephritis, and acute tubular sclerosis with proteinaceous cast formation | Bronchial epithelial denudation, loss of cilia, squamous metaplasia, acute diffuse alveolar damage, and in the late phase acute fibrinous and organizing pneumonia | Diffuse alveolar damage, severe capillary congestion, interstitial mononuclear cell infiltrates, and multinucleated syncytial cells with atypical enlarged pneumocytes, and occasionally microthrombosisa |
| Pathogenesisb | Bronchial lesions are pathologic basis for the respiratory failure; DPP4, the entry receptor widely expressed (epithelial cells in the kidney, alveoli, small intestine, liver, prostate, activated leukocytes); robust and sustained production of proinflammatory cytokines; infects and evades the T cell response; induce apoptosis of both kidney and lung cells through upregulation of Smad7 and FGF2 | Combination of direct virus-induced cytopathic effects and immunopathology induced by a hypercytokinemia or a “cytokine-storm” | Combination of direct virus-induced cytopathic effects, immunologic injury, and microvascular damage induced by cytokines |
aNone of these changes have been shown to be pathognomonic for MERS, SARS, or COVID-19
bAll statements regarding pathogenesis are hypothetical, albeit with some indirect evidence