Putative Natural History of CoViD-19
Journal: 2020/August - International Journal of Molecular Sciences
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: Basigin CD147; Corona Virus Disease 2019 (CoViD-19); Exopeptidase CD26; Peptidase Targeted Immunoregulation (PeTIr); Severe Acute Respiratory Syndrome Corona Virus2 (SARS-CoV2); angiotensin-converting enzyme-2 (ACE2); clustered regularly interspaced short palindromic repeats (CRISPR); cytokine synthesis inhibitory factor (IL10); platelet tissue factor CD142; transferrin receptor CD71; transmembrane protease serine-2 (TMPRSS2).
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Bioinformation 16(5): 398-403

Putative Natural History of CoViD-19

Professor Emeritus, UCLA Center for the Health Sciences, Los Angeles, CA
Francesco Chiappelli moc.liamg@hcraeser.illeppaihC
Received 2020 Apr 15; Accepted 2020 Apr 20.
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.

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),
Abstract

Edited by P Kangueane

Citation: Chiappelli Bioinformation 16(5):398-403 (2020)

References

  • 1. Spreeuwenberg P, et al Am J Epidemiol. 2018;187:2561.[Google Scholar]
  • 2. Vankadari N, Wilce JA. Emerg Microbes Infect. 2020;9:601.
  • 3. Chiappelli F, et al Alcohol Clin Exp Res. . 1995;19:539.[PubMed][Google Scholar]
  • 4. Waumans Y, et al Front. Immunol. . 2015;6:387.[Google Scholar]
  • 5. Ansorge S, et al Clin Chem Lab Med. 2009;47:253.[PubMed][Google Scholar]
  • 6. Sato K, Dang NH. Int J Oncol. 2003;22:481.[PubMed]
  • 7. Chiappelli F, et al Bioinformation . 2020;16:219. DOI 10.6026/97320630016222. [Google Scholar]
  • 8. Hoffmann M, et al Cell. . 2020[PubMed][Google Scholar]
  • 9. Cheng H, et al J Med Virol. 2020[Google Scholar]
  • 10. Coutard B, et al Antiviral Res. 2020;176:104742.[Google Scholar]
  • 11. Wang K, et al BioRxiv. 2020 Doi 10.1101/2020.03.14.988345. [PubMed][Google Scholar]
  • 12. Bian H, et al bioRxiv. 2020 Doi 10.1101/2020.03.21.20040691. [PubMed][Google Scholar]
  • 13. Loughlin EH, et al Antibiot Chemother. 1952;2:171.[PubMed][Google Scholar]
  • 14. Cortegiani A, et al J Crit. Care. Epub. 2020 Doi.org/10.1016/j.jcrc.2020.03.005. [PubMed][Google Scholar]
  • 15. Torigoe M, et al Clin Immunol. 2018;195:1.[PubMed][Google Scholar]
  • 16. Snijder EJ, et al J Mol Biol. 2003;331:991.[Google Scholar]
  • 17. Caly L, et al Antiviral Res. 2020;3:104787.[Google Scholar]
  • 18. Coleman CM, et al J Virol. . 2016;90:8924.[Google Scholar]
  • 19. Sisk JM, et al J Gen Virol. 2018;99:619.[Google Scholar]
  • 20. Totura AL, S Bavari. Expert Opin Drug Discov. 2019;14:397.
  • 21. Zheng S, et al Clin Infect Dis. 2018;66:1054.[PubMed][Google Scholar]
  • 22. Chiappelli F, et al Bioinformation . 2020;16:219. DOI 10.6026/97320630016222. [Google Scholar]
  • 23. Maggi F, et al Clin Microbiol Infect. 2019;25:136.[PubMed][Google Scholar]
  • 24. Nüssing S, et al J Immunol. 2020;204:2308.[PubMed][Google Scholar]
  • 25. Pedersen SF, Ho YC. J Clin Invest. Epub. . 2020
  • 26. Ewart D, et al Semin Arthritis Rheum. 2019;49:e1.[PubMed][Google Scholar]
  • 27. Chiappelli F, et al Bioinformation. 2018;14:201.[Google Scholar]
  • 28. Barkhordarian A, et al Bioinformation. . 2015;11:47.[Google Scholar]
  • 29. Cascella M, et al StatPearls [Internet]. Treasure Island(FL): StatPearls Publishing; 2020[PubMed][Google Scholar]
  • 30. Tang N, et al J Thromb Haemost. Epub. . 2020[PubMed][Google Scholar]
  • 31. Yin S, et al J Thromb Thrombolysis. Epub. . 2020[Google Scholar]
  • 32. Recalcati S. J Eur Acad Dermatol Venereol. Epub. . 2020[PubMed]
  • 33. Adam SS, et al Blood. 2009;113:2878.[PubMed][Google Scholar]
  • 34. Anghel L, et al Int J Mol Sci. . 2020;21pii:E1920.[Google Scholar]
  • 35. Ji HL, et al Physiol Rev. 2020;100:1065.[Google Scholar]
  • 36. Shattuck EC, Muehlenbein MP. Am J Phys Anthropol. . 2015;157:1.[PubMed]
  • 37. Wu P, et al JAMA Ophthalmol. Epub. . 2020[Google Scholar]
  • 38. Madjid M, et al JAMA Cardiol. Epub. . 2020[PubMed][Google Scholar]
  • 39. Li Z, et al Sci China Life Sci. Epub. 2020[Google Scholar]
  • 40. Wu Y, et al Brain Behav Immun. Epub. . 2020[Google Scholar]
  • 41. Gautier JF, Ravussin Y. Obesity (Silver Spring).Epub. 2020
  • 42. Nguyen HC, et al J Clin Med. 2020;9pii:E965.[Google Scholar]
  • 43. Chiappelli F. Bioinformation. 2020;16:288. DOI 10.6026/97320630016288.
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