An Introduction to SARS Coronavirus 2; Comparative Analysis with MERS and SARS Coronaviruses: A Brief Review
-
Mahsa TAHERIZADEH
,
Alireza TABIBZADEH
,
Mahshid PANAHI
,
Fahimeh SAFARNEZHAD TAMESHKEL
,
Mahsa GOLAHDOOZ
,
Mohammad Hadi KARBALAIE NIYA
Abstract
Since the 1970 the replication and pathogenesis mechanism of different coronaviruses have been studded.. In 2002-2003, SARS (Severe Acute Respiratory Syndrome coronavirus) in China emerged which resulted in 8098 cases and 774 deaths. About 10 years later in 2012, the MERS (Middle East Respiratory Syndrome coronavirus) spread in Middle Eastern countries and leads to infection in 2465 cases. In Dec 2019, another acute respiratory disease caused by a novel coronavirus named SARS-2 emerged in Wuhan, China. The virus is assumed to be mainly transmitted by respiratory droplets. Travels and communications leads to high prevalence of COVID-19 (Coronavirus Disease 2019) in the world, and currently in Iran. The current review was conducted to compare the virus structure, genome organization, virus life cycle, pathogenesis and prediction the future of COVID-19.
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21. Lu R, Zhao X, Li J et al (2020). Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. The Lancet, 395(10224):565-74.
22. Zhu Z, Zhang Z, Chen W et al (2018). Predicting the receptor-binding domain usage of the coronavirus based on kmer frequency on spike protein. Infect Genet Evol, 61:183-4.
23. Zhao L, Jha BK, Wu A et al (2012). Antagonism of the interferon-induced OAS-RNase L pathway by murine coronavirus ns2 protein is required for virus replication and liver pathology. Cell Host Microbe, 11(6):607-16.
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29. Xu Y, Cole DK, Lou Z et al (2004). Construct design, biophysical, and biochemical characterization of the fusion core from mouse hepatitis virus (a coronavirus) spike protein. Protein Expr Purif , 38(1):116-22.
30. Supekar VM, Bruckmann C, Ingallinella P et al (2004). Structure of a proteolytically resistant core from the severe acute respiratory syndrome coronavirus S2 fusion protein. Proc Natl Acad Sci U S A, 101(52):17958-63.
31. Donoghue M, Hsieh F, Baronas E et al (2000).A novel angiotensin-converting enzyme–related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9. Circ Res, 87(5):E1-9.
32. Belouzard S, Chu VC, Whittaker GR (2009). Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites. Proc Natl Acad Sci U S A, 106(14): 5871–5876.
33. Boonacker E, Van Noorden CJ (2003). The multifunctional or moonlighting protein CD26/DPPIV. Eur J Cell Biol, 82(2):53-73.
34. Millet JK, Whittaker GR. (2014). Host cell entry of Middle East respiratory syndrome coronavirus after two-step, furin-mediated activation of the spike protein. Proc Natl Acad Sci U S A, 111(42):15214-9.
35. Huang C, Wang Y, Li X et al (2020). Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet, 395(10223):497-506.
36. Peiris M, Guan Y, Yuen K. (2005), Severe acute respiratory syndrome. 1st ed. Blackwell Pub, pp.: 72-76.
37. Liu J, Wu P, Gao F et al (2010). Novel immunodominant peptide presentation strategy: a featured HLA-A* 2402-restricted cytotoxic T-lymphocyte epitope stabilized by intrachain hydrogen bonds from severe acute respiratory syndrome coronavirus nucleocapsid protein. J Virol, 84(22):11849-57.
38. Keicho N, Itoyama S, Kashiwase K et al (2009). Association of human leukocyte antigen class II alleles with severe acute respiratory syndrome in the Vietnamese population. Hum Immunol, 70(7):527-31.
39. Xu Z, Shi L, Wang Y et al (2020). Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med, 1;8(4):420-2.
40. Williams AE, Chambers RC. (2014). The mercurial nature of neutrophils: still an enigma in ARDS? Am J Physiol Lung Cell Mol Physiol, 306(3):L217-L30.
41. Cameron MJ, Bermejo-Martin JF, Danesh A et al (2008). Human immunopathogenesis of severe acute respiratory syndrome (SARS). Virus Res, 133(1):13-9.
42. Min C-K, Cheon S, Ha N-Y et al (2016). Comparative and kinetic analysis of viral shedding and immunological responses in MERS patients representing a broad spectrum of disease severity. Sci Rep, 6: 25359.
43. Ding Y, He L, Zhang Q, Huang Z et al (2004). Organ distribution of severe acute respiratory syndrome (SARS) associated coronavirus (SARS‐CoV) in SARS patients: implications for pathogenesis and virus transmission pathways. The Journal of Pathology, 203(2):622-30.
44. Xu J, Zhong S, Liu J et al (2005). Detection of severe acute respiratory syndrome coronavirus in the brain: potential role of the chemokine mig in pathogenesis. Clin Infect Dis, 41(8):1089-96.
45. Netland J, Meyerholz DK, Moore S et al (2008). Severe acute respiratory syndrome coronavirus infection causes neuronal death in the absence of encephalitis in mice transgenic for human ACE2. J Virol, 82(15):7264-75.
46. Li K, Wohlford-Lenane C, Perlman S et a (2016). Middle East respiratory syndrome coronavirus causes multiple organ damage and lethal disease in mice transgenic for human dipeptidyl peptidase 4. J Infect Dis, 213(5):712-22.
47. Li Y-C, Bai W-Z, Hirano N et al (2012). Coronavirus infection of rat dorsal root ganglia: ultrastructural characterization of viral replication, transfer, and the early response of satellite cells. Virus Res, 163(2):628-35.
48. Li YC, Bai WZ, Hirano N et al (2013). Neurotropic virus tracing suggests a membranous‐coating‐mediated mechanism for transsynaptic communication. J Comp Neurol, 521(1):203-12.
49. Wang D, Hu B, Hu C et al (2020). Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus–infected pneumonia in Wuhan, China. Jama, doi: 10.1001.
50. Hoffmann M, Kleine-Weber H, Krueger N et al (2020). The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells. BioRxiv, doi.org/10.1101/2020.01.31.929042
51. Iwata-Yoshikawa N, Okamura T, Shimizu Y et al (2019). TMPRSS2 contributes to virus spread and immunopathology in the airways of murine models after coronavirus infection. J Virol, 93(6):e01815-18.
52. Zhou Y, Vedantham P, Lu K, et al (2015). Protease inhibitors targeting coronavirus and filovirus entry. Antiviral Res, 116:76-84.
53. Kuba K, Imai Y, Rao S et al (2005). A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus–induced lung injury. Nat Med, 11(8):875-9.
54. Zhang R, Pan Y, Fanelli V et al (2015). Mechanical stress and the induction of lung fibrosis via the midkine signaling pathway. Am J Respir Crit Care Med, 192(3):315-23.
55. World Health Organization (WHO). Coronavirus disease (COVID-2019) situation reports. Available from: https://www.who.int/emergencies/diseases/novel-coronavirus-2019/situation-reports
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57. Organization WH. Coronavirus disease 2019 (COVID-19) situation report–34. Geneva, Switzerland: World Health Organization; 2020. Available from: https://www.who.int/emergencies/diseases/novel-coronavirus-2019/situation-reports
58. Belouzard S, Millet JK, Licitra BN, Whittaker GR (2012). Mechanisms of coronavirus cell entry mediated by the viral spike protein. Viruses, 4(6):1011-33.
2. Lau SK, Lee P, Tsang AK et al (2011). Molecular epidemiology of human coronavirus OC43 reveals evolution of different genotypes over time and recent emergence of a novel genotype due to natural recombination. J Virol, 85(21):11325-37.
3. Tyrrell D, Bynoe M, Hoorn B (1968). Cultivation of" difficult" viruses from patients with common colds. Br Med J, (5592): 606–610.
4. Gerna G, Campanini G, Rovida F et al (2006). Genetic variability of human coronavirus OC43‐, 229E‐, and NL63‐like strains and their association with lower respiratory tract infections of hospitalized infants and immunocompromised patients. J Med Virol, 78(7):938-49.
5. Woo PC, Lau SK, Li KS et al (2006). Molecular diversity of coronaviruses in bats. Virology, 351(1):180-7.
6. Peiris J, Lai S, Poon L et al (2003).Coronavirus as a possible cause of severe acute respiratory syndrome. The Lancet, 361(9366):1319-25.
7. Spaan W, Cavanagh D, Horzinek M (1988). Coronaviruses: structure and genome expression. J Gen Virol, 69(12):2939-52.
8. Balboni A, Battilani M, Prosperi S (2012). The SARS-like coronaviruses: the role of bats and evolutionary relationships with SARS coronavirus. J Microbiol Sci, 35(1):1-16.
9. Peiris JSM, Chu C-M, Cheng VC-C, et al (2003). Clinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia: a prospective study. Lancet, 361(9371):1767-72.
10. Khan G. (2013). A novel coronavirus capable of lethal human infections: an emerging picture. Virol J, 10(1):66.
11. Zaki AM, Van Boheemen S, Bestebroer TM et al (2012). Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia. N Engl J Med, 367(19):1814-20.
12. Azhar EI, Hui DSC, Memish ZA et al (2019). The Middle East Respiratory Syndrome (MERS). Infect Dis Clin North Am, 33(4):891-905.
13. Hui D, Madani T, Ntoumi F et al (2020). The continuing 2019-nCoV epidemic threat of novel coronaviruses to global health-The latest 2019 novel coronavirus outbreak in Wuhan, China. Int J Infect Dis, 91:264-266.
14. McIntosh, K., Hirsch, M.S. and Bloom, A. (2020). Coronavirus Disease 2019 (COVID-19), UpToDate. Available from: https://www.uptodate.com/contents/coronavirus-disease-2019-covid-19-epidemiology-virology-clinical-features-diagnosis-and-prevention
15. World Health Organization (2020). WHO Disease outbreak news: Novel Coronavirus–Republic of Korea (ex-China). January 21, 2020. Available from: https://www.who.int/csr/don/21-january-2020-novel-coronavirus-republic-of-korea-ex-china/en/
16. Liu, S.-L.; Saif, L. (2020). Emerging Viruses without Borders: The Wuhan Coronavirus. Viruses, 12, 130.
17. Song Z, Xu Y, Bao L et al (2019). From SARS to MERS, thrusting coronaviruses into the spotlight. Viruses, 11(1):59.
18. Cui J, Li F, Shi Z-L (2019). Origin and evolution of pathogenic coronaviruses. Nat Rev Microbiol, 17(3):181-92.
19. Dhama K, Sharun K, Tiwari, et al (2020). Coronavirus Disease 2019 – COVID-19. Preprints (doi: 10.20944/preprints202003.0001.v2).
20. Wrapp D, Wang N, Corbett KS et al (2020). Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation. Science, 13;367(6483):1260-3.
21. Lu R, Zhao X, Li J et al (2020). Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. The Lancet, 395(10224):565-74.
22. Zhu Z, Zhang Z, Chen W et al (2018). Predicting the receptor-binding domain usage of the coronavirus based on kmer frequency on spike protein. Infect Genet Evol, 61:183-4.
23. Zhao L, Jha BK, Wu A et al (2012). Antagonism of the interferon-induced OAS-RNase L pathway by murine coronavirus ns2 protein is required for virus replication and liver pathology. Cell Host Microbe, 11(6):607-16.
24. Hoffmann M, Kleine-Weber H, Schroeder S et al (2020). SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell, 181(2): 271-280.
25. Glowacka I, Bertram S, Müller MA et al (2011). Evidence that TMPRSS2 activates the severe acute respiratory syndrome coronavirus spike protein for membrane fusion and reduces viral control by the humoral immune response. J Virol, 85(9):4122-34.
26. Zhou P, Yang X-L, Wang X-G et al (2020). Discovery of a novel coronavirus associated with the recent pneumonia outbreak in humans and its potential bat origin. BioRxiv, doi: 10.1038/s41586-020-2012-7.
27. Yang Y, Peng F, Wang R et al (2020). The deadly coronaviruses: The 2003 SARS pandemic and the 2020 novel coronavirus epidemic in China. J Autoimmun, 109:102434.
28. Bosch BJ, van der Zee R, de Haan CA, Rottier PJ (2003). The coronavirus spike protein is a class I virus fusion protein: structural and functional characterization of the fusion core complex. J Virol, 77(16):8801-11.
29. Xu Y, Cole DK, Lou Z et al (2004). Construct design, biophysical, and biochemical characterization of the fusion core from mouse hepatitis virus (a coronavirus) spike protein. Protein Expr Purif , 38(1):116-22.
30. Supekar VM, Bruckmann C, Ingallinella P et al (2004). Structure of a proteolytically resistant core from the severe acute respiratory syndrome coronavirus S2 fusion protein. Proc Natl Acad Sci U S A, 101(52):17958-63.
31. Donoghue M, Hsieh F, Baronas E et al (2000).A novel angiotensin-converting enzyme–related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9. Circ Res, 87(5):E1-9.
32. Belouzard S, Chu VC, Whittaker GR (2009). Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites. Proc Natl Acad Sci U S A, 106(14): 5871–5876.
33. Boonacker E, Van Noorden CJ (2003). The multifunctional or moonlighting protein CD26/DPPIV. Eur J Cell Biol, 82(2):53-73.
34. Millet JK, Whittaker GR. (2014). Host cell entry of Middle East respiratory syndrome coronavirus after two-step, furin-mediated activation of the spike protein. Proc Natl Acad Sci U S A, 111(42):15214-9.
35. Huang C, Wang Y, Li X et al (2020). Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet, 395(10223):497-506.
36. Peiris M, Guan Y, Yuen K. (2005), Severe acute respiratory syndrome. 1st ed. Blackwell Pub, pp.: 72-76.
37. Liu J, Wu P, Gao F et al (2010). Novel immunodominant peptide presentation strategy: a featured HLA-A* 2402-restricted cytotoxic T-lymphocyte epitope stabilized by intrachain hydrogen bonds from severe acute respiratory syndrome coronavirus nucleocapsid protein. J Virol, 84(22):11849-57.
38. Keicho N, Itoyama S, Kashiwase K et al (2009). Association of human leukocyte antigen class II alleles with severe acute respiratory syndrome in the Vietnamese population. Hum Immunol, 70(7):527-31.
39. Xu Z, Shi L, Wang Y et al (2020). Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med, 1;8(4):420-2.
40. Williams AE, Chambers RC. (2014). The mercurial nature of neutrophils: still an enigma in ARDS? Am J Physiol Lung Cell Mol Physiol, 306(3):L217-L30.
41. Cameron MJ, Bermejo-Martin JF, Danesh A et al (2008). Human immunopathogenesis of severe acute respiratory syndrome (SARS). Virus Res, 133(1):13-9.
42. Min C-K, Cheon S, Ha N-Y et al (2016). Comparative and kinetic analysis of viral shedding and immunological responses in MERS patients representing a broad spectrum of disease severity. Sci Rep, 6: 25359.
43. Ding Y, He L, Zhang Q, Huang Z et al (2004). Organ distribution of severe acute respiratory syndrome (SARS) associated coronavirus (SARS‐CoV) in SARS patients: implications for pathogenesis and virus transmission pathways. The Journal of Pathology, 203(2):622-30.
44. Xu J, Zhong S, Liu J et al (2005). Detection of severe acute respiratory syndrome coronavirus in the brain: potential role of the chemokine mig in pathogenesis. Clin Infect Dis, 41(8):1089-96.
45. Netland J, Meyerholz DK, Moore S et al (2008). Severe acute respiratory syndrome coronavirus infection causes neuronal death in the absence of encephalitis in mice transgenic for human ACE2. J Virol, 82(15):7264-75.
46. Li K, Wohlford-Lenane C, Perlman S et a (2016). Middle East respiratory syndrome coronavirus causes multiple organ damage and lethal disease in mice transgenic for human dipeptidyl peptidase 4. J Infect Dis, 213(5):712-22.
47. Li Y-C, Bai W-Z, Hirano N et al (2012). Coronavirus infection of rat dorsal root ganglia: ultrastructural characterization of viral replication, transfer, and the early response of satellite cells. Virus Res, 163(2):628-35.
48. Li YC, Bai WZ, Hirano N et al (2013). Neurotropic virus tracing suggests a membranous‐coating‐mediated mechanism for transsynaptic communication. J Comp Neurol, 521(1):203-12.
49. Wang D, Hu B, Hu C et al (2020). Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus–infected pneumonia in Wuhan, China. Jama, doi: 10.1001.
50. Hoffmann M, Kleine-Weber H, Krueger N et al (2020). The novel coronavirus 2019 (2019-nCoV) uses the SARS-coronavirus receptor ACE2 and the cellular protease TMPRSS2 for entry into target cells. BioRxiv, doi.org/10.1101/2020.01.31.929042
51. Iwata-Yoshikawa N, Okamura T, Shimizu Y et al (2019). TMPRSS2 contributes to virus spread and immunopathology in the airways of murine models after coronavirus infection. J Virol, 93(6):e01815-18.
52. Zhou Y, Vedantham P, Lu K, et al (2015). Protease inhibitors targeting coronavirus and filovirus entry. Antiviral Res, 116:76-84.
53. Kuba K, Imai Y, Rao S et al (2005). A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus–induced lung injury. Nat Med, 11(8):875-9.
54. Zhang R, Pan Y, Fanelli V et al (2015). Mechanical stress and the induction of lung fibrosis via the midkine signaling pathway. Am J Respir Crit Care Med, 192(3):315-23.
55. World Health Organization (WHO). Coronavirus disease (COVID-2019) situation reports. Available from: https://www.who.int/emergencies/diseases/novel-coronavirus-2019/situation-reports
56. Control CfD, Prevention. Interim pre-pandemic planning guidance: community strategy for pandemic influenza mitigation in the United States. Retrieved March. 2007;21:2007. Available from: https://www.cdc.gov/flu/pandemic-resources/pdf/community_mitigation-sm.pdf
57. Organization WH. Coronavirus disease 2019 (COVID-19) situation report–34. Geneva, Switzerland: World Health Organization; 2020. Available from: https://www.who.int/emergencies/diseases/novel-coronavirus-2019/situation-reports
58. Belouzard S, Millet JK, Licitra BN, Whittaker GR (2012). Mechanisms of coronavirus cell entry mediated by the viral spike protein. Viruses, 4(6):1011-33.
| Files | ||
| Issue | Vol 49 No Supple 1 (2020) | |
| Section | Review Article(s) | |
| DOI | https://doi.org/10.18502/ijph.v49iS1.3667 | |
| Keywords | ||
| Pandemic COVID-19; Viral infection | ||
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How to Cite
1.
TAHERIZADEH M, TABIBZADEH A, PANAHI M, SAFARNEZHAD TAMESHKEL F, GOLAHDOOZ M, KARBALAIE NIYA MH. An Introduction to SARS Coronavirus 2; Comparative Analysis with MERS and SARS Coronaviruses: A Brief Review. Iran J Public Health. 2020;49(Supple 1):30-37.
