Etiological and immunopathogenetic aspects of multiorgan failure development in coronavirus disease (COVID-19)

Authors

DOI:

https://doi.org/10.14739/2310-1210.2024.4.302379

Keywords:

SARS-CoV-2 virus, receptor of angiotensin-converting enzyme 2, endothelium, interferon, cytokines

Abstract

The COVID-19 epidemic has already come to be seen as an emergency of international concern. This relates not only to the wide occurrence of the infection, but also to a fairly high mortality rate, currently more than 6.5 million deaths in the world.

The aim of this study was to analyze, generalize and systematize the currently available literary data on the study of the novel coronavirus infection pathogenesis in the human body and to determine key changes that occur after the SARS-CoV-2 penetration into cells. In this way to target physicians primarily based on the pathogenetic processes that occur in the human body, syndromes and symptom complexes that are observed in treatments.

Results. The article presents a literature review demonstrating that the specific interaction between the virus and somatic cells is the triggering mechanism for the pathogenesis of coronavirus infection. The main route for SARS-CoV-2 entry into the body is the angiotensin-converting enzyme 2 (ACE2) receptor, which is expressed not only in type 2 alveolar epithelial cells, but also in cells of the kidney, heart, blood vessels and gastrointestinal tract, including endotheliocytes and pericytes. Expression of the ACE2 receptor has also been shown in various structures and parts of the brain, cells of the conjunctiva, limbus, cornea and cells of the substantia propria. A high expression of the ACE2 receptor has been found in the epithelial cells of the oral mucosa, salivary glands, tonsils and tongue. These factors explain a possible involvement of different organs and systems in the development of multiorgan failure.

Conclusions. In the development of multiorgan disfunction, two components are important: first, direct cell tropism and viral load, that may be unique in each patient. Secondly, it is the development of immune-mediated reactions to infected cells. Under conditions of hyperimmune inflammation, that is, the development of cytokine storm, acute respiratory distress syndrome progresses, and multiple organ failure develops. Endothelial damage is directly involved in the pathophysiology of this process, that results in the development of endothelial dysfunction, disruption of microcirculation, as well as perivascular inflammation, which aggravates damage to the endothelium and can lead to thrombus formation.

The use of modern knowledge about the immunopathogenesis of COVID-19 would help to estimate the risk for severe infection and the possible development of complications, allowing for the timely implementation of effective pathogenetic therapy.

Author Biographies

T. V. Ashcheulova, Kharkiv National Medical University, Ukraine

MD, PhD, DSc, Professor, Head of the Department of Propedeutics of Internal Medicine, Nursing and Bioethics

N. M. Herasymchuk, Kharkiv National Medical University, Ukraine

MD, PhD, Associate Professor of the Department of Propedeutics of Internal Medicine, Nursing and Bioethics

O. A. Kochubiei, Kharkiv National Medical University, Ukraine

MD, PhD, Associate Professor of the Department of Propedeutics of Internal Medicine, Nursing and Bioethics

U. S. Herasymchuk, Kharkiv National Medical University, Ukraine

MD, PhD, Assistant of the Department of Endocrinology and Pediatric Endocrinology

References

  1. Coronavirus disease 2019 (COVID-19): situation report – 36 [Internet]. Geneva: World Health Organization, 2020 Feb 25 [cited 2024 Jun 18]. Available from: https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200225-sitrep-36-covid-19.pdf?sfvrsn=2791b4e0_2
  2. WHO Director-General's opening remarks at the media briefing on COVID-19 - 11 March 2020 [Internet]. 2020 Mar 11. [cited 2024 Jun 18]. Available from: https://www.who.int/director-general/speeches/detail/who-director-general-s-opening-remarks-at-the-media-briefing-on-covid-19---11-march-2020
  3. Pericàs JM, Hernandez-Meneses M, Sheahan TP, Quintana E, Ambrosioni J, Sandoval E, et al. COVID-19: from epidemiology to treatment. Eur Heart J. 2020;41(22):2092-112. doi: https://doi.org/10.1093/eurheartj/ehaa46
  4. Sadigov R. Rapid Growth of the World Population and Its Socioeconomic Results. ScientificWorldJournal. 2022 Mar 23;2022:8110229. doi: https://doi.org/10.1155/2022/8110229
  5. World Health Organisation. WHO Coronavirus (COVID-19) Dashboard [Internet]. 2022 [cited 2024 Jun 14]. Available from: https://covid19.who.int/
  6. Oronsky B, Larson C, Hammond TC, Oronsky A, Kesari S, Lybeck M, Reid TR. A Review of Persistent Post-COVID Syndrome (PPCS). Clin Rev Allergy Immunol. 2023 Feb;64(1):66-74. doi: https://doi.org/10.1007/s12016-021-08848-3
  7. Astuti I, Ysrafil. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2): An overview of viral structure and host response. Diabetes Metab Syndr. 2020;14(4):407-12. doi: https://doi.org/10.1016/j.dsx.2020.04.020
  8. Wang MY, Zhao R, Gao LJ, Gao XF, Wang DP, Cao JM. SARS-CoV-2: Structure, Biology, and Structure-Based Therapeutics Development. Front Cell Infect Microbiol. 2020;10:587269. doi: https://doi.org/10.3389/fcimb.2020.587269
  9. Cui J, Li F, Shi ZL. Origin and evolution of pathogenic coronaviruses. Nat Rev Microbiol. 2019;17(3):181-92. doi: https://doi.org/10.1038/s41579-018-0118-9
  10. Lan J, Ge J, Yu J, Shan S, Zhou H, Fan S, et al. Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor. Nature. 2020;581(7807):215-20. doi: https://doi.org/10.1038/s41586-020-2180-5
  11. Cerutti G, Guo Y, Zhou T, Gorman J, Lee M, Rapp M, et al. Potent SARS-CoV-2 neutralizing antibodies directed against spike N-terminal domain target a single supersite. Cell Host Microbe. 2021;29(5):819-833.e7. doi: https://doi.org/10.1016/j.chom.2021.03.005
  12. McCallum M, De Marco A, Lempp FA, Tortorici MA, Pinto D, Walls AC, et al. N-terminal domain antigenic mapping reveals a site of vulnerability for SARS-CoV-2. Cell. 2021;184(9):2332-47. doi: https://doi.org/10.1016/j.cell.2021.03.028
  13. Xing L, Xu X, Xu W, Liu Z, Shen X, Zhou J, et al. A Five-Helix-Based SARS-CoV-2 Fusion Inhibitor Targeting Heptad Repeat 2 Domain against SARS-CoV-2 and Its Variants of Concern. Viruses. 2022;14(3):597. doi: https://doi.org/10.3390/v14030597
  14. Guo L, Lin S, Chen Z, Cao Y, He B, Lu G. Targetable elements in SARS-CoV-2 S2 subunit for the design of pan-coronavirus fusion inhibitors and vaccines. Signal Transduct Target Ther. 2023;8(1):197. doi: https://doi.org/10.1038/s41392-023-01472-x
  15. Ma X, Zou F, Yu F, Li R, Yuan Y, Zhang Y, et al. Nanoparticle Vaccines Based on the Receptor Binding Domain (RBD) and Heptad Repeat (HR) of SARS-CoV-2 Elicit Robust Protective Immune Responses. Immunity. 2020;53(6):1315-30.e9. doi: https://doi.org/10.1016/j.immuni.2020.11.015
  16. Pack SM, Peters PJ. SARS-CoV-2–Specific Vaccine Candidates; the Contribution of Structural Vaccinology. Vaccines. 2022;10(2):236. doi: https://doi.org/10.3390/vaccines10020236
  17. Yan W, Zheng Y, Zeng X, He B, Cheng W. Structural biology of SARS-CoV-2: open the door for novel therapies. Signal Transduct Target Ther. 2022;7(1):26. doi: https://doi.org/10.1038/s41392-022-00884-5
  18. Choi JH, Zhang X, Zhang C, Dai DL, Luo J, Ladak R, et al. SARS-CoV-2 impairs interferon production via NSP2-induced repression of mRNA translation. BioRxiv. 2022;2022:01. doi: https://doi.org/10.1101/2022.01.19.476693
  19. 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):271-280.e8. doi: https://doi.org/10.1016/j.cell.2020.02.052
  20. Wrapp D, Wang N, Corbett KS, Goldsmith JA, Hsieh CL, Abiona O, et al. Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation. Science. 2020;367(6483):1260-3. doi: https://doi.org/10.1126/science.abb2507
  21. Zhao S, Lin Q, Ran J, Musa SS, Yang G, Wang W, et al. Preliminary estimation of the basic reproduction number of novel coronavirus (2019-nCoV) in China, from 2019 to 2020: A data-driven analysis in the early phase of the outbreak. Int J Infect Dis. 2020;92:214-7. doi: https://doi.org/10.1016/j.ijid.2020.01.050
  22. Zou X, Chen K, Zou J, Han P, Hao J, Han Z. Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection. Front Med. 2020;14(2):185-92. doi: https://doi.org/10.1007/s11684-020-0754-0
  23. Borges do Nascimento IJ, Cacic N, Abdulazeem HM, Von Groote TC, Jayarajah U, Weerasekara I, et al. Novel Coronavirus Infection (COVID-19) in humans: A Scoping Review and Meta-Analysis. J Clin Med. 2020;9(4):941. doi: https://doi.org/10.3390/jcm9040941
  24. Robinson FA, Mihealsick RP, Wagener BM, Hanna P, Poston MD, Efimov IR, et al. Role of angiotensin-converting enzyme 2 and pericytes in cardiac complications of COVID-19 infection. Am J Physiol Heart Circ Physiol. 2020;319(5):1059-68. doi: https://doi.org/10.1152/ajpheart.00681.2020
  25. Chen R, Wang K, Yu J, Howard D, French L, Chen Z, et al. The Spatial and Cell-Type Distribution of SARS-CoV-2 Receptor ACE2 in the Human and Mouse Brains. Front Neurol. 2021;11:573095. doi: https://doi.org/10.3389/fneur.2020.573095
  26. Huang N, Perez P, Kato T, Mikami Y, Okuda K, Gilmore RC, et al. Integrated single-cell atlases reveal an oral SARS-CoV-2 infection and transmission axis. medRxiv [Preprint]. 2020 Oct 27:2020.10.26.20219089. doi: https://doi.org/10.1101/2020.10.26.20219089
  27. Hou YJ, Okuda K, Edwards CE, Martinez DR, Asakura T, Dinnon KH, et al. SARS-CoV-2 Reverse Genetics Reveals a Variable Infection Gradient in the Respiratory Tract. Cell. 2020;182(2): 429-446.e14. doi: https://doi.org/10.1016/j.cell.2020.05.042
  28. Lu CW, Liu XF, Jia ZF. 2019-nCoV transmission through the ocular surface must not be ignored. Lancet. 2020;395(10224):e39. doi: https://doi.org/10.1016/S0140-6736(20)30313-5
  29. Li JP, Lam DS, Chen Y, Ting DS. Novel Coronavirus disease 2019 (COVID-19): The importance of recognising possible early ocular manifestation and using protective eyewear. Br J Ophthalmol. 2020;104(3):297-8. doi: https://doi.org/10.1136/bjophthalmol-2020-315994
  30. Dadras O, Afsahi AM, Pashaei Z, Mojdeganlou H, Karimi A, Habibi P, et al. The relationship between COVID‐19 viral load and disease severity: A systematic review. Immun Inflamm Dis. 2021;10(3):e580. doi: https://doi.org/10.1002/iid3.580
  31. South AM, Diz DI, Chappell MC. COVID-19, ACE2, and the cardiovascular consequences. Am J Physiol Heart Circ Physiol. 2020;318:H1084-90. doi: https://doi.org/10.1152/ajpheart.00217.2020
  32. Nugent MA. The future of the COVID-19 pandemic: How good (or bad) can the SARS-CoV2 spike protein get? Cells. 2022;11(5):855. doi: https://doi.org/10.3390/cells11050855
  33. Sriram K, Insel PA. A hypothesis for pathobiology and treatment of COVID‐19 : The centrality of ACE1/ACE2 imbalance. Br J Pharmacol. 2020;177(21):4825-44. doi: https://doi.org/10.1111/bph.15082
  34. Letko M, Marzi A, Munster V. Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses. Nat Microbiol. 2020;5(4):562-9. doi: https://doi.org/10.1038/s41564-020-0688-y
  35. Najafi K, Maroufi P, Khodadadi E, Zeinalzadeh E, Ganbarov K, Asgharzadeh M, et al. SARS-CoV-2 receptor ACE2 and molecular pathway to enter target cells during infection. Rev Med Microbiol. 2020;33(1):e105-13. doi: https://doi.org/10.1097/MRM.0000000000000237
  36. 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. Вiorxiv. 2020;2020.03. doi: https://doi.org/10.1101/2020.03.14.988345
  37. Behl T, Kaur I, Aleya L, Sehgal A, Singh S, Sharma N, et al. CD147-spike protein interaction in COVID-19: Get the ball rolling with a novel receptor and therapeutic target. Sci Total Environ. 2022;808:152072. doi: https://doi.org/10.1016/j.scitotenv.2021.152072
  38. Han X, Zhou Z, Fei L, Sun H, Wang R, Chen Y, et al. Construction of a human cell landscape at single-cell level. Nature. 2020;581(7808):303-9. doi: https://doi.org/10.1038/s41586-020-2157-4
  39. Chen IY, Moriyama M, Chang MF, Ichinohe T. Severe Acute Respiratory Syndrome Coronavirus Viroporin 3a Activates the NLRP3 Inflammasome. Front Microbiol. 2019;10:441068. doi: https://doi.org/10.3389/fmicb.2019.00050
  40. Zhao C, Zhao W. NLRP3 Inflammasome-A Key Player in Antiviral Responses. Front Immunol. 2020;11:211. doi: https://doi.org/10.3389/fimmu.2020.00211
  41. da Costa LS, Outlioua A, Anginot A, Akarid K, Arnoult D. RNA viruses promote activation of the NLRP3 inflammasome through cytopathogenic effect-induced potassium efflux. Cell Death Dis. 2019;10(5):346. doi: https://doi.org/10.1038/s41419-019-1579-0
  42. Sánchez-Rodríguez R, Munari F, Angioni R, Venegas F, Agnellini A, Castro-Gil MP, et al. Targeting monoamine oxidase to dampen NLRP3 inflammasome activation in inflammation. Cell Mol Immunol. 2021;18(5):1311-3. doi: https://doi.org/10.1038/s41423-020-0441-8
  43. Fung SY, Yuen KS, Ye ZW, Chan CP, Jin DY. A tug-of-war between severe acute respiratory syndrome coronavirus 2 and host antiviral defence: lessons from other pathogenic viruses. Emerg Microbes Infect. 2020;9(1):558-70. doi: https://doi.org/10.1080/22221751.2020.1736644
  44. Cavalcante-Silva LH, Carvalho DC, Lima ÉD, Galvão JG, da Silva JS, Sales-Neto JM, et al. Neutrophils and COVID-19: The road so far. Int Immunopharmacol. 2021;90:107233. doi: https://doi.org/10.1016/j.intimp.2020.107233
  45. Van der Made CI, Simons A, Schuurs-Hoeijmakers J, van den Heuvel G, Mantere T, Kersten S, et al. Presence of genetic variants among young men with severe COVID-19. JAMA. 2020;324(7):663-73. doi: https://doi.org/10.1001/jama.2020.13719
  46. Khongthaw B, Dulta K, Chauhan PK, Kumar V, Ighalo JO. Lycopene: a therapeutic strategy against coronavirus disease 19 (COVID-19). Inflammopharmacology. 2022;30(6):1955-76. doi: https://doi.org/10.1007/s10787-022-01061-4
  47. Meidaninikjeh S, Sabouni N, Marzouni HZ, Bengar S, Khalili A, Jafari R. Monocytes and macrophages in COVID-19: Friends and foes. Life Sci. 2021;269:119010. doi: https://doi.org/10.1016/j.lfs.2020.119010
  48. Zhu H, Ding Y, Zhang Y, Ding X, Zhao J, Ouyang W, et al. CTRP3 induces an intermediate switch of CD14++CD16+ monocyte subset with anti‑inflammatory phenotype. Exp Ther Med. 2020;19(3):2243-51. doi: https://doi.org/10.3892/etm.2020.8467
  49. Li Z, Yi Y, Luo X, Xiong N, Liu Y, Li S, et al. Development and clinical application of a rapid IgM‐IgG combined antibody test for SARS‐CoV‐2 infection diagnosis. J Med Virol. 2020;92(9):1518-24. doi: https://doi.org/10.1002/jmv.25727
  50. Zhang L, Liu Y. Potential interventions for novel coronavirus in China: A systematic review. J Med Virol. 2020;92(5):479-90. doi: https://doi.org/10.1002/jmv.25707
  51. Kaivola J, Nyman TA, Matikainen S. Inflammasomes and SARS-CoV-2 Infection. Viruses. 2021;13(12):2513. doi: https://doi.org/10.3390/v13122513
  52. Kim JS, Lee JY, Yang JW, Lee KH, Effenberger M, Szpirt W, et al. Immunopathogenesis and treatment of cytokine storm in COVID-19. Theranostics. 2021;11(1):316-29. doi: https://doi.org/10.7150/thno.49713
  53. Thomas S, Smatti MK, Ouhtit A, Cyprian FS, Almaslamani MA, Thani AA, et al. Antibody-Dependent Enhancement (ADE) and the role of complement system in disease pathogenesis. Mol Immunol. 2022;152:172-82. doi: https://doi.org/10.1016/j.molimm.2022.11.010
  54. Rabaan AA, Al-Ahmed SH, Muhammad J, Khan A, Sule AA, Tirupathi R, et al. Role of inflammatory cytokines in COVID-19 patients: A review on molecular mechanisms, immune functions, immunopathology and immunomodulatory drugs to counter cytokine storm. Vaccines. 2021;9(5):436. doi: https://doi.org/10.3390/vaccines9050436
  55. Qudus MS, Tian M, Sirajuddin S, Liu S, Afaq U, Wali M, et al. The roles of critical pro‐inflammatory cytokines in the drive of cytokine storm during SARS‐CoV‐2 infection. J Med Virol. 2023;95(4):e28751 doi: https://doi.org/10.1002/jmv.28751
  56. Makaremi S, Asgarzadeh A, Kianfar H, Mohammadnia A, Asghariazar V, Safarzadeh E. The role of IL-1 family of cytokines and receptors in pathogenesis of COVID-19. Inflamm Res. 2022;71(7):923-47. doi: https://doi.org/10.1007/s00011-022-01596-w
  57. Liu F, Li L, Xu M, Wu J, Luo D, Zhu Y, et al. Prognostic value of interleukin-6, C-reactive protein, and procalcitonin in patients with COVID-19. J Clin Virol. 2020;127:104370 doi: https://doi.org/10.1016/j.jcv.2020.104370
  58. Yang P, Ding Y, Xu Z, Pu R, Li P, Yan J, et al. Epidemiological and clinical features of COVID-19 patients with and without pneumonia in Beijing, China. Medrxiv. 2020. doi: https://doi.org/10.1101/2020.02.28.20028068
  59. Han H, Ma Q, Li C, Liu R, Zhao L, Wang W, et al. Profiling serum cytokines in COVID-19 patients reveals IL-6 and IL-10 are disease severity predictors. Emerg Microbes Infect. 2020;9(1):1123-30. doi: https://doi.org/10.1080/22221751.2020.1770129
  60. Lu L, Zhang H, Dauphars DJ, He YW A potential role of interleukin 10 in COVID-19 pathogenesis. Trends Immunol. 2021;42(1):3-5. doi: https://doi.org/10.1016/j.it.2020.10.012
  61. Satış H, Özger HS, Aysert Yıldız P, Hızel K, Gulbahar Ö, Erbaş G, et al. Prognostic value of interleukin-18 and its association with other inflammatory markers and disease severity in COVID-19. Cytokine. 2021;137:155302. doi: https://doi.org/10.1016/j.cyto.2020.155302
  62. Costela-Ruiz VJ, Illescas-Montes R, Puerta-Puerta JM, Ruiz C, Melguizo-Rodríguez L. SARS-CoV-2 infection: The role of cytokines in COVID-19 disease. Cytokine Growth Factor Rev. 2020;54:62-75. doi: https://doi.org/10.1016/j.cytogfr.2020.06.001
  63. Naidu SA, Clemens RA, Naidu AS. SARS-CoV-2 infection dysregulates host iron (Fe)-redox homeostasis (Fe-RH): role of Fe-redox regulators, ferroptosis inhibitors, anticoagulants, and iron-chelators in COVID-19 control. J Diet Suppl. 2023;20(2):312-71. doi: https://doi.org/10.1080/19390211.2022.2075072
  64. Xu S, Ilyas I, Little PJ, Li H, Kamato D, Zheng X, et al. Endothelial Dysfunction in Atherosclerotic Cardiovascular Diseases and Beyond: From Mechanism to Pharmacotherapies. Pharmacol Rev. 2021;73(3):924-67. doi: https://doi.org/10.1124/pharmrev.120.000096
  65. Chia PY, Teo A, Yeo TW. Overview of the assessment of endothelial function in humans. Front Med. 2020;7:542567. doi: https://doi.org/10.3389/fmed.2020
  66. Balta S. Endothelial dysfunction and inflammatory markers of vascular disease. Curr Vasc Pharmacol. 2021;19(3):243-9. doi: https://doi.org/10.2174/1570161118666200421142542
  67. Varga Z, Flammer AJ, Steiger P, Haberecker M, Andermatt R, Zinkernagel AS, et al. Endothelial cell infection and endotheliitis in COVID-19. Lancet. 2020;395(10234):1417-8. doi: https://doi.org/10.1016/s0140-6736(20)30937-5
  68. Wang M, Hao H, Leeper NJ, Zhu L. Thrombotic Regulation From the Endothelial Cell Perspectives. Arterioscler Thromb Vasc Biol. 2018;38(6):e90-e95. doi: https://doi.org/10.1161/atvbaha.118.310367
  69. Nizzoli ME, Merati G, Tenore A, Picone C, Consensi E, Perotti L, et al. Circulating endothelial cells in COVID ‐19. Am J Hematol. 2020;95(8):E187. doi: https://doi.org/10.1002/ajh.25881
  70. Russo A, Tellone E, Barreca D, Ficarra S, Laganà G. Implication of COVID-19 on Erythrocytes Functionality: Red Blood Cell Biochemical Implications and Morpho-Functional Aspects. Int J Mol Sci. 2022;23(4):2171. doi: https://doi.org/10.3390/ijms23042171
  71. Gibson PG, Qin L, Puah SH. COVID ‐19 acute respiratory distress syndrome (ARDS): clinical features and differences from typical pre‐ COVID ‐19 ARDS. Med J Aust. 2020;213(2):54. doi: https://doi.org/10.5694/mja2.50674
  72. Recktenwald SM, Simionato G, Lopes MG, Gamboni F, Dzieciatkowska M, Meybohm P, et al. Cross-talk between red blood cells and plasma influences blood flow and omics phenotypes in severe COVID-19. Elife. 2022;11:e81316. doi: https://doi.org/10.7554/eLife.81316
  73. Revzin MV, Raza S, Warshawsky R, D’Agostino C, Srivastava NC, Bader AS, et al. Multisystem Imaging Manifestations of COVID-19, Part 1: Viral Pathogenesis and Pulmonary and Vascular System Complications. RadioGraphics. 2020;40(6):1574-99. doi: https://doi.org/10.1148/rg.2020200149
  74. Xie L, Lin Y, Deng Y, Lei B. The Effect of SARS-CoV-2 on the Spleen and T Lymphocytes. Viral Immunol. 2021;34(6):416-20. 73. doi: https://doi.org/10.1089/vim.2020.0320
  75. Chen L, Li X, Chen M, Feng Y, Xiong C. The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovasc Res. 2020;116(6):1097-100. doi: https://doi.org/10.1093/cvr/cvaa078
  76. He L, Mäe MA, Sun Y, Muhl L, Nahar K, Liébanas EV, et al. Pericyte-specific vascular expression of SARS-CoV-2 receptor ACE2–implications for microvascular inflammation and hypercoagulopathy in COVID-19 patients. BioRxiv. 2020;2020-05. doi: https://doi.org/10.1101/2020.05.11.088500
  77. Cardot-Leccia N, Hubiche T, Dellamonica J, Burel-Vandenbos F, Passeron T. Pericyte alteration sheds light on micro-vasculopathy in COVID-19 infection. Intensive Care Med. 2020;46(9):1777-8. doi: https://doi.org/10.1007/s00134-020-06147-7
  78. Arachchillage DR, Laffan M. Abnormal coagulation parameters are associated with poor prognosis in patients with novel coronavirus pneumonia. J Thromb Haemost. 2020;18(5):1233-4. doi: https://doi.org/10.1111/jth.14820
  79. Fogarty H, Townsend L, Ni Cheallaigh C, Bergin C, Martin‐Loeches I, Browne P, et al. COVID19 coagulopathy in Caucasian patients. Br J Haematol. 2020;189(6):1044-9. doi: https://doi.org/10.1111/bjh.16749
  80. Petrey AC, Qeadan F, Middleton EA, Pinchuk IV, Campbell RA, Beswick EJ. Cytokine release syndrome in COVID‐19: Innate immune, vascular, and platelet pathogenic factors differ in severity of disease and sex. J Leukoc Biol. 2021;109(1):55-66. doi: https://doi.org/10.1002/JLB.3COVA0820-410RRR
  81. Helms J, Tacquard C, Severac F, Leonard-Lorant I, Ohana M, Delabranche X, et al. High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study. Intensive Care Med. 2020;46(6):1089-98. doi: https://doi.org/10.1007/s00134-020-06062-x
  82. O'Sullivan JM, Gonagle DM, Ward SE, Preston RJ, O'Donnell JS. Endothelial cells orchestrate COVID-19 coagulopathy. Lancet Haematol. 2020;7(8):e553-5. doi: https://doi.org/10.1016/S2352-3026(20)30215-5
  83. Flaumenhaft R, Enjyoji K, Schmaier AA. Vasculopathy in COVID-19. Blood. 2022;140(3):222-35. doi: https://doi.org/10.1182/blood.2021012250
  84. Loghmani H, Conway EM. Exploring traditional and nontraditional roles for thrombomodulin. Blood. 2018;132(2):148-58. doi: https://doi.org/10.1182/blood-2017-12-768994
  85. Won T, Wood MK, Hughes DM, Talor MV, Ma Z, Schneider J, et al. Endothelial thrombomodulin downregulation caused by hypoxia contributes to severe infiltration and coagulopathy in COVID-19 patient lungs. EbioMedicine. 2022;75:103812. doi: https://doi.org/10.1016/j.ebiom.2022.103812
  86. Vaduganathan M, Vardeny O, Michel T, McMurray JJ, Pfeffer MA, Solomon SD. Renin-Angiotensin-Aldosterone System Inhibitors in Patients with Covid-19. New Engl J Med. 2020;382(17):1653-9. doi: https://doi.org/10.1056/NEJMsr2005760
  87. COVID-19 rapid guideline: managing the long-term effects of COVID-19. London: National Institute for Health and Care Excellence (NICE); 2020 Dec 18. Available from: https://www.nice.org.uk/guidance/ng188
  88. Pierce JD, Shen Q, Cintron SA, Hiebert JB. Post-COVID-19 Syndrome. Nurs Res. 2022;71(2):164-74. doi: https://doi.org/10.1097/NNR.0000000000000565
  89. Pavli A, Theodoridou M, Maltezou HC. Post-COVID Syndrome: Incidence, Clinical Spectrum, and Challenges for Primary Healthcare Professionals. Arch Med Res. 2021;52(6):575-81. doi: https://doi.org/10.1016/j.arcmed.2021.03.010
  90. Inciardi RM, Adamo M, Lupi L, Cani DS, Di Pasquale M, Tomasoni D, et al. Characteristics and outcomes of patients hospitalized for COVID-19 and cardiac disease in Northern Italy. Eur Heart J. 2020;41(19):1821-9. doi: https://doi.org/10.1093/eurheartj/ehaa388
  91. Inciardi RM, Lupi L, Zaccone G, Italia L, Raffo M, Tomasoni D, et al. Cardiac Involvement in a Patient With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. 2020;5(7):819-24. doi: https://doi.org/10.1001/jamacardio.2020.1096
  92. Guo T, Fan Y, Chen M, Wu X, Zhang L, He T, et al. Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. 2020;5(7):811-8. doi: https://doi.org/10.1001/jamacardio.2020.1017
  93. Bonow RO, Fonarow GC, O’Gara PT, Yancy CW. Association of Coronavirus Disease 2019 (COVID-19) With Myocardial Injury and Mortality. JAMA Cardiol. 2020;5(7):751-3. doi: https://doi.org/10.1001/jamacardio.2020.1105
  94. Heneka MT, Golenbock D, Latz E, Morgan D, Brown R. Immediate and long-term consequences of COVID-19 infections for the development of neurological disease. Alzheimers Res & Ther. 2020;12(1):1-3. doi: https://doi.org/10.1186/s13195-020-00640-3
  95. Lasso G, Honig B, Shapira SD. A Sweep of Earth’s Virome Reveals Host-Guided Viral Protein Structural Mimicry and Points to Determinants of Human Disease. Cell Syst. 2021;12(1):82-91. doi: https://doi.org/10.1016/j.cels.2020.09.006
  96. Yapici-Eser H, Koroglu YE, Oztop-Cakmak O, Keskin O, Gursoy A, Gursoy-Ozdemir Y. Neuropsychiatric Symptoms of COVID-19 Explained by SARS-CoV-2 Proteins’ Mimicry of Human Protein Interactions. Front Hum Neurosci. 202;15:656313. doi: https://doi.org/10.3389/fnhum.2021.656313
  97. Paniz‐Mondolfi A, Bryce C, Grimes Z, Gordon RE, Reidy J, Lednicky J, et al. Central nervous system involvement by severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2). J Med Virol. 2020;92(7):699-702. doi: https://doi.org/10.1002/jmv.25915
  98. Rogers JP, Chesney E, Oliver D, Pollak TA, McGuire P, Fusar-Poli P, et al. Psychiatric and neuropsychiatric presentations associated with severe coronavirus infections: a systematic review and meta-analysis with comparison to the COVID-19 pandemic. Lancet Psychiatry. 2020;7(7):611-27. doi: https://doi.org/10.1016/S2215-0366(20)30203-0
  99. Varatharaj A, Thomas N, Ellul MA, Davies NW, Pollak TA, Tenorio EL, et al. Neurological and neuropsychiatric complications of COVID-19 in 153 patients: a UK-wide surveillance study. Lancet Psychiatry. 2020;7(10):875-82. doi: https://doi.org/10.1016/S2215-0366(20)30287-X
  100. Ortelli P, Ferrazzoli D, Sebastianelli L, Engl M, Romanello R, Nardone R, et al. Neuropsychological and neurophysiological correlates of fatigue in post-acute patients with neurological manifestations of COVID-19: Insights into a challenging symptom. J Neurol Sci. 2021;420:117271. doi: https://doi.org/10.1016/j.jns.2020.117271
  101. Del Brutto OH, Wu S, Mera RM, Costa AF, Recalde BY, Issa NP. Cognitive decline among individuals with history of mild symptomatic SARS‐CoV‐2 infection: A longitudinal prospective study nested to a population cohort. Eur J Neurol. 2021;28(10):3245-53. doi: https://doi.org/10.1111/ene.14775
  102. Amalakanti S, Arepalli KV, Jillella JP. Cognitive assessment in asymptomatic COVID-19 subjects. VirusDisease. 2021;32(1):146-9. doi: https://doi.org/10.1007/s13337-021-00663-w
  103. Hampshire A, Trender W, Chamberlain SR, Jolly AE, Grant JE, Patrick F, et al. Cognitive deficits in people who have recovered from COVID-19. EClinicalMedicine. 2021;39:101044. doi: https://doi.org/10.1016/j.eclinm.2021.101044
  104. Miskowiak K, Johnsen S, Sattler S, Nielsen S, Kunalan K, Rungby J, et al. Cognitive impairments four months after COVID-19 hospital discharge: Pattern, severity and association with illness variables. Eur Neuropsychopharmacol. 2021;46:39-48. doi: https://doi.org/10.1016/j.euroneuro.2021.03.019
  105. Mao L, Jin H, Wang M, Hu Y, Chen S, He Q, et al. Neurologic Manifestations of Hospitalized Patients With Coronavirus Disease 2019 in Wuhan, China. JAMA Neurol. 2020;77(6):683-90. doi: https://doi.org/10.1001/jamaneurol.2020.1127
  106. Edeas M, Saleh J, Peyssonnaux C. Iron: Innocent bystander or vicious culprit in COVID-19 pathogenesis? Int J Infect Dis. 2020;97:303-5. doi: https://doi.org/10.1016/j.ijid.2020.05.110
  107. Bellastella G, Maiorino MI, Esposito K. Endocrine complications of COVID-19: what happens to the thyroid and adrenal glands? J Endocrinol Investig. 2020;43(8):1169-70. doi: https://doi.org/10.1007/s40618-020-01311-8
  108. Zhang J, Tecson KM, McCullough PA. Endothelial dysfunction contributes to COVID-19-associated vascular inflammation and coagulopathy. Rev Cardiovasc Med. 2020;21(3):315-9. doi: https://doi.org/10.31083/j.rcm.2020.03.126
  109. Baig AM, Khaleeq A, Ali U, Syeda H. Evidence of the COVID-19 Virus Targeting the CNS: Tissue Distribution, Host-Virus Interaction, and Proposed Neurotropic Mechanisms. ACS Chem Neurosci. 2020;11(7):995-8. doi: https://doi.org/10.1021/acschemneuro.0c00122
  110. Norouzi M, Miar P, Norouzi S, Nikpour P. Nervous System Involvement in COVID-19: a Review of the Current Knowledge. Mol Neurobiol. 2021;58:3561-74. doi: https://doi.org/10.1007/s12035-021-02347-4
  111. Zhang B, Zhou X, Zhu C, Song Y, Feng F, Qiu Y, et al. Immune Phenotyping Based on the Neutrophil-to-Lymphocyte Ratio and IgG Level Predicts Disease Severity and Outcome for Patients With COVID-19. Front Mol Biosci. 2020;7:157. doi: https://doi.org/10.3389/fmolb.2020.00157
  112. Mehta P, McAuley DF, Brown M, Sanchez E, Tattersall RS, Manson JJ. COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet. 2020;395(10229):1033-4. doi: https://doi.org/10.1016/S0140-6736(20)30628-0
  113. 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. doi: https://doi.org/10.1007/s12250-020-00207-4
  114. Skalny A, Rink L, Ajsuvakova O, Aschner M, Gritsenko V, Alekseenko S, et al. Zinc and respiratory tract infections: Perspectives for COVID‑19 (Review). Int J Mol Med. 2020;46(1):17-26. doi: https://doi.org/10.3892/ijmm.2020.4575
  115. Zarifian A, Zamiri Bidary M, Arekhi S, Rafiee M, Gholamalizadeh H, Amiriani A, et al. Gastrointestinal and hepatic abnormalities in patients with confirmed COVID‐19: A systematic review and meta‐analysis. J Med Virol. 2021;93(1):336-50. doi: https://doi.org/10.1002/jmv.26314
  116. Huang N, Pérez P, Kato T, Mikami Y, Okuda K, Gilmore RC, et al. SARS-CoV-2 infection of the oral cavity and saliva. Nat Med. 2021;27(5):892-903. doi: https://doi.org/10.1038/s41591-021-01296-8
  117. Xiao F, Tang M, Zheng X, Liu Y, Li X, Shan H. Evidence for Gastrointestinal Infection of SARS-CoV-2. Gastroenterology. 2020;158(6):1831-3. doi: https://doi.org/10.1053/j.gastro.2020.02.055
  118. Liang W, Feng Z, Rao S, Xiao C, Xue X, Lin Z, et al. Diarrhoea may be underestimated: a missing link in 2019 novel coronavirus. Gut. 2020;69(6):1141-3. doi: https://doi.org/10.1136/gutjnl-2020-320832
  119. Wu Y, Guo C, Tang L, Hong Z, Zhou J, Dong X, et al. Prolonged presence of SARS-CoV-2 viral RNA in faecal samples. Lancet Gastroenterol Hepatol. 2020;5(5):434-5. doi: https://doi.org/10.1016/S2468-1253(20)30083-2
  120. Singh J, Sharma T. Liver injury among coronavirus disease patients. J Surg Spec Rural Pract. 2022;3(1):6-8. doi: https://doi.org/10.4103/jssrp.jssrp_21_21
  121. Nardo AD, Schneeweiss‐Gleixner M, Bakail M, Dixon ED, Lax SF, Trauner M. Pathophysiological mechanisms of liver injury in COVID‐19. Liver Int.2021;41(1):20-32. doi: https://doi.org/10.1111/liv.14730
  122. Wang F, Wang H, Fan J, Zhang Y, Wang H, Zhao Q. Pancreatic Injury Patterns in Patients With Coronavirus Disease 19 Pneumonia. Gastroenterology. 2020;159(1):367-70. doi: https://doi.org/10.1053/j.gastro.2020.03.055
  123. Kartika H, Suhaimi N, Ali Z, Suprapti, Effendi I, Hudari H, et al. Recent Evidence on Acute Kidney Injury in COVID-19 Patients: A Narrative Review. Biosci Medicina. 2022;6(10):2313-21. doi: https://doi.org/10.37275/bsm.v6i10.599
  124. Chong WH, Saha BK. Relationship Between Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and the Etiology of Acute Kidney Injury (AKI). Am J Med Sci. 2020;361(3):287-96. doi: https://doi.org/10.1016/j.amjms.2020.10.025
  125. Helms L, Marchiano S, Stanaway IB, Hsiang TY, Juliar BA, Saini S, et al. Cross-validation of SARS-CoV-2 responses in kidney organoids and clinical populations. JCI Insight. 2021;6(24):e154882. doi: https://doi.org/10.1172/jci.insight.154882
  126. Gavriilaki E, Anyfanti P, Gavriilaki M, Lazaridis A, Douma S, Gkaliagkousi E. Endothelial Dysfunction in COVID-19: Lessons Learned from Coronaviruses. Curr Hypertens Rep. 2020;22:63. https://doi.org/doi: https://doi.org/10.1007/s11906-020-01078-6
  127. Wang C, Yu C, Novakovic VA, Xie R, Shi J. Circulating Microparticles in the Pathogenesis and Early Anticoagulation of Thrombosis in COVID-19 With Kidney Injury. Front Cell Dev Biol. 2022;9:784505. doi: https://doi.org/10.3389/fcell.2021.784505
  128. Głowacka M, Lipka S, Młynarska E, Franczyk B, Rysz J. Acute Kidney Injury in COVID-19. Int J Mol Sci. 2021;22(15):8081. doi: https://doi.org/10.3390/ijms22158081

Downloads

Published

2024-07-17

How to Cite

1.
Ashcheulova TV, Herasymchuk NM, Kochubiei OA, Herasymchuk US. Etiological and immunopathogenetic aspects of multiorgan failure development in coronavirus disease (COVID-19). Zaporozhye Medical Journal [Internet]. 2024Jul.17 [cited 2026May13];26(4):331-45. Available from: https://zmj.zsmu.edu.ua/article/view/302379

Issue

Vol. 26 No. 4 (2024)

Section

Review

License

Authors who publish with this journal agree to the following terms:

Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.  Лицензия Creative Commons