[Home ] [Archive]   [ فارسی ]  
:: Main :: About :: Current Issue :: Archive :: Search :: Submit :: Contact ::
Main Menu
Journal Information::
Indexing Sources::
Guide for Authors::
Online Submission::
Articles archive::
For Reviewers::
Contact us::
Basic and Clinical Biochemistry and Nutrition
Search in website

Advanced Search
Receive site information
Enter your Email in the following box to receive the site news and information.
:: Volume 26, Issue 3 (Bimonthly 2022) ::
Feyz 2022, 26(3): 342-352 Back to browse issues page
Investigation the reasons for varying the severity of COVID-19 from person to person: A review study
Mohsen Rahmani , Bahare Nikoozar , Mahboobeh Golchin , Marziyeh Tavalaee , Mehdi Hajian , Mohammad Hossein Nasr-Esfahani
Department of Animal Biotechnology, Reproductive Biomedicine Research Center, Royan Institute for Biotechnology, ACECR, Isfahan, I.R. Iran. , Tavalaee.royan@gmail.com
Abstract:   (1524 Views)
Background: COVID-19 is caused by the SARS-COV-2 virus and mainly affects the lung tissue. In addition, other tissues are attacked by the virus. Reports have shown that clinical manifestations in Covid-19 patients vary from asymptomatic to acute respiratory symptoms in the lung and septic shock affecting the immune system in other organs. This review article aimed to investigate the molecular mechanisms associated with SARS-COV-2 pathogenicity and the relationship between these mechanisms and the severity of various clinical manifestations in patients.
Materials and Methods: Published articles by researchers in PubMed and Google scholar databases from 2019 to 2021 were collected and reviewed based on the keywords SARS-COV-2, COVID-19 and disease severity.
Results: After entering the SARS-COV-2 virus into the body and the activation of the immune system for reasons such as increased NET production, oxidative stress, activation of cell death pathways including ferroptosis and finally the explosion of cytokine storm and pyroptosis, exacerbate the severity of the disease and increase mortality. In addition, the molecular expression of NLRP3 can play a major role in the development of cytokine storms in patients, some depend on their immune system to fight the virus due to the proliferation of NLRP3 and other destructive molecular mechanisms, thus showing the different severity of the disease.
Conclusion: Individuals in the community show varying degrees of Covid-19 disease depending on the different reactions of their immune systems. Various cellular and molecular mechanisms appear to be activated in sufferers that NLRP3 expression plays a large role.
Keywords: SARS-COV-2, COVID-19, Immune system, NLRP3, NETosis, Cytokine storm
Full-Text [PDF 745 kb]   (912 Downloads)    
Type of Study: Review | Subject: medicine, paraclinic
Received: 2021/11/20 | Revised: 2022/09/10 | Accepted: 2022/06/11 | Published: 2022/07/30
1. Fahmi I. World Health Organization coronavirus disease 2019 (Covid-19) situation report. DroneEmprit. 2019.
2. Gerotziafas GT, Catalano M, Colgan M-P, Pecsvarady Z, Wautrecht JC, Fazeli B, et al. Guidance for the management of patients with vascular disease or cardiovascular risk factors and COVID-19: position paper from VAS-European Independent Foundation in Angiology/Vascular Medicine. Thromb Haemost 2020; 120(12): 1597-628.
3. Boettler T, Marjot T, Newsome PN, Mondelli MU, Maticic M, Cordero E, et al. Impact of COVID-19 on the care of patients with liver disease: EASL-ESCMID position paper after 6 months of the pandemic. JHEP Rep 2020; 2(5).
4. Wu L, O'Kane AM, Peng H, Bi Y, Motriuk-Smith D, Ren J. SARS-CoV-2 and cardiovascular complications: from molecular mechanisms to pharmaceutical management. Biochem pharmacol. 2020; 178: 114114
5. Trottein F, Sokol H. Potential causes and consequences of gastrointestinal disorders during a SARS-CoV-2 infection. Cell Rep 2020; 32(3): 107915.
6. Hoffmann M, Kleine-Weber H, Schroeder S, Krüger N, Herrler T, Erichsen S, et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 2020; 181(2): 271-80. e8.
7. Tian S, Hu N, Lou J, Chen K, Kang X, Xiang Z, et al. Characteristics of COVID-19 infection in Beijing. J Infect 2020; 80(4): 401-6.
8. Meng J, Xiao G, Zhang J, He X, Ou M, Bi J, et al. Renin-angiotensin system inhibitors improve the clinical outcomes of COVID-19 patients with hypertension. Emerg Microbes Infect 2020; 9(1): 757-60.
9. Agrawal H, Das N, Nathani S, Saha S, Saini S, Kakar SS, Roy P. An assessment on impact of COVID-19 infection in a gender specific manner. Stem Cell Rev Rep. 2020; 17(1): 94-112.
10. Rahimi Z, Moradi M, Nasri H. A systematic review of the role of renin angiotensin aldosterone system genes in diabetes mellitus, diabetic retinopathy and diabetic neuropathy. Journal of research in medical sciences: J Res Med Sci 2014; 19(11): 1090.
11. Merad M, Martin JC. Pathological inflammation in patients with COVID-19: a key role for monocytes and macrophages. Nat Rev Immunol 2020; 20(6): 355-62.
12. Beltrán-García J, Osca-Verdegal R, Pallardó FV, Ferreres J, Rodríguez M, Mulet S, et al. Oxidative stress and inflammation in COVID-19-associated sepsis: the potential role of anti-oxidant therapy in avoiding disease progression. Antioxidants (Basel) 2020; 9(10): 936.
13. Schönrich G, Raftery MJ. Neutrophil extracellular traps go viral. Front Immunol 2016; 7: 366.
14. Masso-Silva JA, Moshensky A, Lam MT, Odish M, Patel A, Xu L, et al. Increased peripheral blood neutrophil activation phenotypes and NETosis in critically ill COVID-19 patients. Clin Infect Dis 2021; ciab437.
15. Middleton EA, He XY, Denorme F, Campbell RA, Ng D, Salvatore SP, et al. Neutrophil extracellular traps contribute to immunothrombosis in COVID-19 acute respiratory distress syndrome. Blood 2020; 136(10): 1169-79.
16. Edler C, Schröder AS, Aepfelbacher M, Fitzek A, Heinemann A, Heinrich F, et al. Dying with SARS-CoV-2 infection—an autopsy study of the first consecutive 80 cases in Hamburg, Germany. Int J Legal Med 2020; 134(4): 1275-84.
17. Rabelo LA, Alenina N, Bader M. ACE2–angiotensin-(1–7)–Mas axis and oxidative stress in cardiovascular disease. Hypertens Res 2011; 34(2): 154-60.
18. Rana MM. Cytokine storm in COVID-19: Potential therapeutics for immunomodulation. JRCM 2020; 8(1): 38.
19. Cavezzi A, Troiani E, Corrao S. COVID-19: hemoglobin, iron, and hypoxia beyond inflammation. A narrative review. Clin Pract 2020; 10(2): 24-30.
20. Laforge M, Elbim C, Frère C, Hémadi M, Massaad C, Nuss P, et al. Tissue damage from neutrophil-induced oxidative stress in COVID-19. Nat Rev Immunol 2020; 20(9): 515-516.
21. Ji P, Zhu J, Zhong Z, Li H, Pang J, Li B, Zhang J. Association of elevated inflammatory markers and severe COVID-19: A meta-analysis. Med (Baltimore) 2020; 99(47).
22. Panigrahy D, Gilligan MM, Huang S, Gartung A, Cortés-Puch I, Sime PJ, et al. Inflammation resolution: a dual-pronged approach to averting cytokine storms in COVID-19? Cancer Metastasis Rev. 2020; 39(2):337-40.
23. Guan WJ, Ni ZY, Hu Y, Liang WH, Ou Cq, He JX, et al. Clinical characteristics of (2019) novel coronavirus infection in China. N Engl J Med 2020.
24. Yang X, Yu Y, Xu J, Shu H, Liu H, Wu Y, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med 2020; 8(5): 475-81.
25. Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020; 395(10223): 497-506.
26. Yang M. Cell pyroptosis, a potential pathogenic mechanism of 2019-nCoV infection. Available at SSRN 2020; 3527420.
27. Yang Y, Peng F, Wang R, Guan K, Jiang T, Xu G, et al. The deadly coronaviruses: The 2003 SARS pandemic and the 2020 novel coronavirus epidemic in China. J Autoimmun 2020; 109: 102434.
28. Schultze JL, Aschenbrenner AC. COVID-19 and the human innate immune system. Cell 2021; 184(7): 1671-92.
29. Zhou Y, He C, Wang L, Ge B. Post‐translational regulation of antiviral innate signaling. Eur J Immunol 2017; 47(9): 1414-26.
30. Karki R, Sharma BR, Tuladhar S, Williams EP, Zalduondo L, Samir P, et al. Synergism of TNF-α and IFN-γ Triggers Inflammatory Cell Death, Tissue Damage, and Mortality in SARS-CoV-2 Infection and Cytokine Shock Syndromes. Cell 2021; 184(1): 149.
31. Chen IY, Moriyama M, Chang MF, Ichinohe T. Severe acute respiratory syndrome coronavirus viroporin 3a activates the NLRP3 inflammasome. Front Microbiol 2019; 10: 50.
32. Xu H, Chitre SA, Akinyemi IA, Loeb JC, Lednicky JA, McIntosh MT, et al. SARS-CoV-2 viroporin triggers the NLRP3 inflammatory pathway. Virology 2020.
33. Chan CM, Tsoi H, Chan WM, Zhai S, Wong CO, Yao X, et al. The ion channel activity of the SARS-coronavirus 3a protein is linked to its pro-apoptotic function. Int J Biochem Cell Biol 2009; 41(11): 2232-9.
34. Cagliani R, Forni D, Clerici M, Sironi M. Coding potential and sequence conservation of SARS-CoV-2 and related animal viruses. Infect Genet Evol 2020; 83: 104353.
35. Ahn M, Anderson DE, Zhang Q, Tan CW, Lim BL, Luko K, et al. Dampened NLRP3-mediated inflammation in bats and implications for a special viral reservoir host. Nat Microbiol. 2019; 4(5): 789-99.
36. Van den Berg DF, Te Velde AA. Severe COVID-19: NLRP3 inflammasome dysregulated. Front Immunol 2020; 11: 1580.
37. Fu Y, Cheng Y, Wu Y. Understanding SARS-CoV-2-mediated inflammatory responses: from mechanisms to potential therapeutic tools. Virol Sin 2020; 35(3): 266-71.
38. Imai Y, Kuba K, Rao S, Huan Y, Guo F, Guan B, et al (). Angiotensin-converting enzyme 2 protects from severe acute lung failure. Nature 2005; 436(7047): 112-6.
39. Chakraborty S, Gonzalez J, Edwards K, Mallajosyula V, Buzzanco AS, Sherwood R, et al. Proinflammatory IgG Fc structures in patients with severe COVID-19. Nat Immunol 2021; 22(1): 67-73.
40. Zhang L, Zhang F, Yu W, He T, Yu J, Yi CE, et al. Antibody responses against SARS coronavirus are correlated with disease outcome of infected individuals. J Med Virol 2006; 78(1): 1-8.
41. Liu L, Wei Q, Lin Q, Fang J, Wang H, Kwok H, et al . Anti–spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection. JCI Insight 2019; 4(4).
42. Shattuck EC, Muehlenbein MP. Human sickness behavior: Ultimate and proximate explanations. Am J Phys Anthropol. 2015; 157(1): 1-18.
43. Lara PC, Macías-Verde D, Burgos-Burgos J (). Age-induced NLRP3 Inflammasome over-activation increases lethality of SARS-CoV-2 pneumonia in elderly patients. Aging Dis. 2020; 11(4): 756.
44. Latz E, Duewell P. NLRP3 inflammasome activation in inflammaging. Semin Immunol 2018; 40: 61-73.
45. Bertocchi I, Foglietta F, Collotta D, Eva C, Brancaleone V, Thiemermann C, Collino M. The hidden role of NLRP3 inflammasome in obesity‐related COVID‐19 exacerbations: lessons for drug repurposing. Br J Pharmacol 2020; 177(21): 4921-30.
46. López-Reyes A, Martinez-Armenta C, Espinosa-Valázquez R, Vázquez-Cárdenas P, Cruz-Ramos M, Gomez-Quiroz LE, Martínez-Nava GA. NLRP3 Inflammasome: the stormy link between obesity and COVID-19. Front Immunol 2020; 11: 2875.
47. Samadizadeh S, Masoudi M, Rastegar M, Salimi V, Shahbaz MB, Tahamtan A. COVID-19: Why does disease severity vary among individuals? Respir Med 2021: 106356.
48. Beltrán-García J, Osca-Verdegal R, Pallardó FV, Ferreres J, Rodríguez M, Mulet S. Sepsis and Coronavirus Disease 2019: Common Features and Anti-Inflammatory Therapeutic Approaches. Crit Care Med 2020.
49. Manzanares W, Dhaliwal R, Jiang X, Murch L, Heyland DK. Antioxidant micronutrients in the critically ill: a systematic review and meta-analysis. Crit Care 2012; 16(2): 1-13.
50. Acuña‐Castroviejo D, Escames G, Figueira JC, de la Oliva P, Borobia AM, Acuña‐Fernández C. Clinical trial to test the efficacy of melatonin in COVID‐19. J Pineal Res 2020; 69(3): e12683.
51. Carrasco C, Marchena AM, Holguín‐Arévalo MS, Martín‐Partido G, Rodríguez AB, Paredes SD, Pariente JA. Anti‐inflammatory effects of melatonin in a rat model of caerulein‐induced acute pancreatitis. Cell Biochem Funct 2013; 31(7): 585-90.
52. Cronje HT, Nienaber-Rousseau C, Zandberg L, De Lange Z, Green FR, Pieters M. Fibrinogen and clot-related phenotypes determined by fibrinogen polymorphisms: Independent and IL-6-interactive associations. PLoS One 2017; 12(11): e0187712.
53. Sidelmann JJ, Gram J, Jespersen J, Kluft C. Fibrin clot formation and lysis: basic mechanisms. Semin Thromb Hemost 2000; 26(6): 605-18.
54. Huang Y, Hua J, Yun C, W, Yang Y, Tao J, Deng X, et al. Tranilast directly targets NLRP 3 to treat inflammasome‐driven diseases. EMBO Mol Med 2018; 10(4): e8689.
55. Yang X, Yang LX, Wu J, Guo ML, Zhang Y, Ma SG. Treatment of lidocaine on subacute thyroiditis via restraining inflammatory factor expression and inhibiting pyroptosis pathway. J Cell Biochem 2019; 120(7): 10964-71.
56. Bode C, Peukert K, Schewe JC, Putensen C, Latz E, Steinhagen F. Tetracycline alleviates acute lung injury by inhibition of NLRP3 inflammasome. Eur Respir J 2019; 54: PA2175
Send email to the article author

Add your comments about this article
Your username or Email:


XML   Persian Abstract   Print

Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Rahmani M, Nikoozar B, Golchin M, Tavalaee M, Hajian M, Nasr-Esfahani M H. Investigation the reasons for varying the severity of COVID-19 from person to person: A review study. Feyz 2022; 26 (3) :342-352
URL: http://feyz.kaums.ac.ir/article-1-4509-en.html

Creative Commons License
This open access journal is licensed under a Creative Commons Attribution-NonCommercial ۴.۰ International License. CC BY-NC ۴. Design and publishing by Kashan University of Medical Sciences.
Copyright ۲۰۲۳© Feyz Medical Sciences Journal. All rights reserved.
Volume 26, Issue 3 (Bimonthly 2022) Back to browse issues page
مجله علوم پزشکی فیض Feyz Medical Sciences Journal
Persian site map - English site map - Created in 0.08 seconds with 46 queries by YEKTAWEB 4642