Title
Authors
Francesco Chiappelli
Affiliation
Francesco Chiappelli, Professor Emeritus, UCLA Center for the Health Sciences, Los Angeles, CA
Francesco Chiappelli - Chiappelli.research@gmail.com; *Corresponding author
Article Type
Editorial
Date
Received April 15, 2020; Accepted April 20, 2020; Published May 31, 2020
Abstract
The Severe Acute Respiratory Syndrome Corona Virus2 (SARS-CoV2) is responsible for Corona Virus Disease 2019 (CoViD-19), the pandemic that has afflicted close to two million people worldwide, and has taken the lives of over 120,000 patients since its first report in late December 2019. Per million people globally, the infection rate is close to 250 with a death rate of close to 14 (death rate average global death rate: 6.06%; for comparison, revised estimate of the 1918 influenza pandemic had an average global death rate of 5.4% [1]). About 400,000 SARS-CoV2-positive patients have been declared ‘recovered’, although it is not clear to date what exactly that entails. To be clear, the natural history of SARS-CoV2 infection and of the patho-physiology of CoViD-19 remains shrouded in relative confusion, in part due to the exceedingly virulent nature of the virus, as manifest by its elevated morbidity and mortality, and the fast accumulation of clinical observations and research evidence. Many pieces of a complex puzzle are emerging all at once and their organization into a coherent and cogent picture of the natural history of CoViD-19 is arduous and still wanting. Here, we discuss the recent findings in the context of the available evidence. We propose a putative prediction model of the natural history of CoViD-19. We highlight putative loci and modes of therapeutic intervention that may become beneficial preventive and treatment modalities for individuals at risk of SARS-CoV2 infection and CoViD-19 patients.
Keywords
Corona Virus Disease 2019 (CoViD-19); Severe Acute Respiratory Syndrome Corona Virus2 (SARS-CoV2); Exopeptidase CD26; Peptidase Targeted Immunoregulation (PeTIr); angiotensin-converting enzyme-2 (ACE2); transmembrane protease serine-2 (TMPRSS2); Basigin CD147; clustered regularly interspaced short palindromic repeats (CRISPR); transferrin receptor CD71; platelet tissue factor CD142; cytokine synthesis inhibitory factor (IL10)
Citation
Chiappelli, Bioinformation 16(5): 398-403 (2020)
Edited by
P Kangueane
ISSN
0973-2063
Publisher
License
This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.
