Immunopathogenesis of Pneumonia in COVID-19

Letter to Editor


1 Department of Molecular Medicine, Institute of Medical Biotechnology, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran

2 Chronic Respiratory Diseases Research Center, National Research Institute of Tuberculosis and Lung Diseases (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran

3 Clinical Tuberculosis and Epidemiology Research Center, (NRITLD), Shahid Beheshti University of Medical Sciences, Tehran, Iran

4 Department of Immunology, Faculty of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran


Coronavirus disease 2019 (COVID-19), caused by a member of the Coronaviridae family (SARS-CoV-2), was initially reported in Wuhan, China in late December and spread rapidly around the world, reaching a pandemic level (1). This disease has been diagnosed in almost 4.44 million people globally, resulting in more than 302,000 deaths until 15 May, 2020 (2). In Iran, a total of 115,000 confirmed cases of COVID-19 were reported until May 2020, with a fatality rate of 5.118%. Coronaviruses are enveloped positive-stranded RNA viruses with an approximate size of 80-120 nm. They contain the longest viral RNA genomes of all RNA virus families (3). The whole genome sequence of this novel virus contains 29,903 nucleotides. SARS-CoV-2 is closely related to bat-derived SARS-like coronaviruses, sharing 79% nucleotide identity with SARS-CoV (4, 5). Also, viral capsid proteins, including spike glycoprotein (S protein), play an important role in the cell entry and tropism in patients with COVID-19 (6). Overall, coronaviruses use a variety of receptors to enter the cells. Recent evidence shows high homology between SARS-CoV and SARS-CoV-2, as SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) as its receptor, similar to SARS-CoV (7).