Elements of the dynamics of the immune response to SARS-CoV-2 infection
Keywords:
COVID-19, SARS-CoV-2, immune response, cytokine stormAbstract
Introduction: COVID-19 is the disease caused by the SARS-CoV-2 virus. Though most patients present mild or moderate symptoms, 5% develop severe respiratory syndrome. Awareness of the dynamics of the immune response to SARS-CoV-2 infection is essential for the appropriate management of patients.
Objective: Describe the essential elements of the dynamics of the immune response to SARS-CoV-2 infection.
Methods: A review was conducted of updated literature contained in bibliographic databases. A total 40 publications were consulted. An analysis was performed of the quality and reliability of the papers selected.
Data analysis and integration: In the initial stage of the immune response to SARS-CoV-2 there is a predominance of innate defense mechanisms aimed at eliminating the virus and preventing the progress of the disease toward severity. If the immune system fails to eradicate the virus, immune dysregulation will occur and considerable damage will result from tissue inflammation. Immunotherapy should focus on stimulating the first (protective) stage and delete the second. An appropriate immune response is vital in the combat against coronavirus infections.
Conclusions: The dynamics of the antiviral response in SARS-CoV-2 patients are essential elements conditioning the severity of the disease. Occurrence of the cytokine storm resulting from immune dysregulation has been cited as the primary cause of the severe respiratory syndrome developing in these patients. Better knowledge about the immunopathogenic mechanisms involved is indispensable to develop highly efficient drugs.
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References
1. Zhu N, Zhang D, Wang W, Li X, Yang B, Song J. A Novel Coronavirus from Patients with Pneumonia in China, 2019. N Engl J Med. 2020;382(8):727-33.
2. World Health Organization. Coronavirus disease 2019 (COVID-19) Situation Report – 170. World Health Organization; 2020 [acceso: 01/08/2020]. Disponible en: https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200708-covid-19-sitrep-170.pdf
3. Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395(10223):497-506.
4. Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome Lancet Respir Med. 2020;8(4). DOI: 10.1016/S2213-2600(20)30076-X
5. Lu G, Wang Q, Gao GF. Bat-to-human: Spike features determining “host jump” of coronaviruses SARS-CoV, MERS-CoV, and beyond. Trends Microbiol. 2015;23(8):468-78.
6. Coutard B, Valle C, de Lamballerie X, Canard B, Seidah NG, Decroly E. The spike glycoprotein of the new coronavirus 2019-nCoV contains a furin-like cleavage site absent in CoV of the same clade. Antiviral Research.2020;176:104742. DOI: 10.1016/j.antiviral.2020.104742
7. Belouzard S, Chu VC, Whittaker GR. Activation of the SARS coronavirus spike protein via sequential proteolytic cleavage at two distinct sites. ProcNatl Acad Sci USA. 2009;106:5871-6.
8. Bassi DE, Zhang J, Renner C, Klein-Szanto AJ. Targeting proprotein convertases in furin-rich lung cancer cells results in decreased in vitro and in vivo growth. Mol Carcinog. 2017;56:1182-8.
9. Kido H, Okumura Y, Takahashi E, Pan HY, Wang S, Yao D,et al.Role of host cellular proteases in the pathogenesis of influenza and influenza-induced multiple organ failure. BiochimBiophys Acta. 2012;1824(1):186-94.
10. Hoffmann M, Kleine-Weber H, Krüger N, Müller M, Drosten C, Pöhlmann S. SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor. Cell. 2020;181:1-10. DOI: 10.1016/j.cell.2020.02.052
11. Lu R, Zhao X, Li J, Niu P, Yang B. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding. Lancet. 2020;395:565-74. DOI: 10.1016/S0140-6736(20)30251-8
12. Walls AC, Park Y-J, Tortorici MA, Wall A, McGuire AT, Veesler D. Structure, Function, and Antigenicity of the SARS-CoV-2 Spike Glycoprotein. Cell. 2020;180:1-12. DOI: 10.1016/j.cell.2020.02.058
13. Jia HP, Look DC, Shi L, Hickey M. ACE2 Receptor Expression and Severe Acute Respiratory Syndrome Coronavirus Infection Depend on Differentiation of Human Airway Epithelia. J Virol. 2005;79(23):14614-21.
14. Turner AJ, Hiscox JA, Hooper NM. ACE2: from vasopeptidase to SARS virus receptor. Trends Pharmacol Sci. 2004;25:291-4.
15. Soro-Paavonen A, Gordin D, Forsblom C, Rosengard-Barlund M. Circulating ACE2 activity is increased in patients with type 1diabetes and vascular complications. J Hypert. 2012;30:375-83.
16. Guan W-J, Liang W-H, Zhao Y. Comorbidity and its impact on 1590 patients with Covid-19 in China: A Nationwide Analysis. Eur Respir J. 2020;55:2000547. DOI: 10.1183/13993003.00547-2020
17. Iacono K, Brown AL, Greene MI, SaouafSJ. CD147inmunoglobulin superfamily receptor funtion and role in pathology. Exp Mol Pathol. 2007 [acceso: 22/06/2020]; 83(3):283-95. Disponible en: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2211739/pdf/nihms35343.pdf
18. Wang K, Chen W, Zhou YS, Lian JQ, Zhang Z, Du P,et al.SARS-CoV-2 invades host cells via a novel route: CD147-spike protein. Biorxiv. 2020 [acceso: 29/06/2020]. Preprint. DOI: 10.1101/2020.03.14.988345
19. Li Q, Guan X, Wu P. Early transmission dynamics in Wuhan, China, of novel coronavirus-infected pneumonia. N Engl J Med. 2020;38:1199-107. DOI: 10.1056/NEJMoa2001316
20. Shi Y, Wang Y, Shao C, Huang J. COVID-19 infection: the perspectives on immune responses. Cell Death Differ. 2020;27(5):1451-54.DOI: 10.1038/s41418-020-0530-3
21. Pérez O, Vega I. Inmunología en el humano sano. La Habana: ECIMED, 2017. Capítulo II.
22. Kawai T, Akira S. The role of pattern-recognition receptors in innate immunity: update on toll-like receptors. Nat Immunol. 2010;11(5):373-84.
23. SnijderEJ, van der Meer Y, Zevenhoven-Dobbe J. Ultrastructure and origin of membrane vesicles associated with the severe acute respiratory syndrome coronavirus replication complex. J Virol. 2006;80:5927-40. DOI: 10.1128/JVI.02501-05
24. Lessler J, Reich NG, Brookmeyer R, Perl TM, Nelson KE, Cummings DA. Incubation periods of acute respiratory viral infections: a systematic review. Lancet Infect Dis. 2009 [acceso: 28/06/2020];9(5):291-300. Disponible en: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4327893/pdf/main.pdf
25. Huang L, Zhang X, Zhang X, Wei Z, Zhang L, Xu Jet al.Rapid asymptomatic transmission of COVID-19 during the incubation period demonstrating strong infectivity in a cluster of youngsters aged 16-23 years outside Wuhan and characteristics of young patients with COVID-19: A prospective contact-tracing study. J Inf. 2020;80:e1-e13. DOI: 10.1016/j.jinf.2020.03.006
26. Trouillet-Assant S, Viel S, Gaymard A, Pons S, Richard J-C, Perret M, et al. Type I IFN immunoprofiling in COVID-19 patients. J Allergy Clin Immunol. 2020;146(1):206-8. DOI: 10.1016/j.jaci.2020.04.029
27. Sallard E, Lescure F-X, Yazdanpanah Y, Mentre F, Peiffer-Smadja N. Type 1 interferons as a potential treatment against COVID-19. Antiviral Research. 2020;178. DOI: 10.1016/j.antiviral.2020.104791
28. Zhou Q, Chen V, Shannon C, Wei X-S, Xiang X, Wang X,et al.Interferon-α2b Treatment for COVID-19. Front Immunol. 2020;11:1061. DOI: 10.3389/fimmu.2020.01061
29. Zhang G, Nie S, Zhang Z, Zahang Z. Longitudinal Change of SARS-Cov2 Antibodies in Patients with COVID-19. J Inf Dis.2020;222(2):183-88.DOI: 10.1093/infdis/jiaa229
30. Zhao J, Yuan Q, Wang H, Liu W, Liao X, Su Y, et al. Antibody responses to SARS-CoV-2 in patients of novel coronavirus disease 2019. Clin Infect Dis. 2020. Epub ahead of print. DOI: 10.1093/cid/ciaa344
31. Thevarajan I, Nguyen THO, Koutsakos M, Druce J, Caly L. Breadth of concomitant immune responses prior to patient recovery: a case report of non-severe COVID-19. Nat Med. 2020;26(4):453-55. DOI: 10.1038/s41591-020-0819-2
32. Gao T, Hu M, Zhang X, Li H. Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2-mediated complement over-activation. MedRxiv. 2020.Preprint.DOI: 10.1101/2020.03.29.20041962
33. McGonaglea D, Sharif K, O'Regand A, Bridgewood C. The Role of Cytokines including Interleukin-6 in COVID-19 induced Pneumonia and Macrophage Activation Syndrome-Like Disease. Autoimmunity Reviews. 2020;19(6):102537. DOI: 10.1016/j.autrev.2020.102537
34. Qin C, Zhou L, Hu Z, Zhang S, Yang S. Dysregulation of Immune Response in Patients with Coronavirus 2019 (COVID-19) in Wuhan,China. Clin Infect Dis. 2020;71(15):762-8. DOI: 10/1093/cid/ciaa248
35. Tan L, Wang Q, Zhang D, Ding J. Lymphopenia predicts disease severity of COVID-19: a descriptive and predictive study. Sig Trans Targ Ther. 2020;5(33). DOI: 10.1038/s41392-020-0148-4
36. Diao B, Wang C, Tan Y, Chen X, Liu Y, NIng L, et al. Reduction and Functional Exhaustion of T Cells in Patients with Coronavirus Disease 2019 (COVID-19) Front Immunol. 2020;11:827. DOI: 10.3389/fimmu.2020.00827
37. Francisco L, Sage P, Sharpe A. The PD-1 pathway in tolerance and autoimmunity. Immunol Rev. 2010;236:219-42. DOI: 10.1111/j.1600-065X.2010.00923
38. Cao X. COVID-19: immunopathology and its implications for therapy. Nat Rev Immunol. 2020;20:269-70. DOI: 10.1038/s41577-020-0308-3
39. Saavedra D, Añé-Kourí A, Sánchez N, Filgueira L, Betancourt J, Herrera C, et al. An Anti-CD6 Monoclonal Antibody (Itolizumab) Reduces Circulating IL-6 in Severe Covid-19 Elderly Patients. Research Square. 2020;17(1):1-8. DOI: 10.21203/rs.3.rs-32335/v1
40. Loganathan S, Athalye SN, Joshi SR. Itolizumab, an anti-CD6 monoclonal antibody, as a potential treatment for COVID-19 complications. Exp Opin Biol Ther. 2020;20(9):1025-31. DOI: 10.1080/14712598.2020.1798399
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