Acta Scientific Microbiology (ASMI) (ISSN: 2581-3226)

Research Article Volume 4 Issue 3

Corticosteroid Actions on COVID-19 and SARS Viral Immune Pathology; A Review Article

SM Rathnasiri Bandara1 and HMMTB Herath2

1Dip in Psychiatry, Medical Officer, Kandy General Hospital, Sri Lanka
2Senior Registrar in National Hospital of Colombo, Sri Lanka

*Corresponding Author: Herath, Senior Registrar in National Hospital of Colombo, Sri Lanka.

Received: October 14, 2020; Published: Febuary 27, 2021

×

Abstract

  Only few studies are available to evaluate the effectiveness of corticosteroids in SARS and SARS-CoV-2. Corticosteroids is a hormone, as well as a drug, having therapeutic levels and lethal doses, so needs to balance the doses accordingly to the disease. Here we discuss the use of steroids in SARS, MERS and COVID-19 with reviewing the pharmacological and immunological basis of steroids in virus pathology. Steroids can be beneficial in these viral infections by suppressing SARS-CoV induced antibodies, T cells, B cells, cytokines, chemokines, complement signaling, antibody-dependent enhancement, vascular and hematological manifestations, viral replication and COX-2/PGE2 pathways. Steroids can also protects against cell apoptosis and enhance tissue recovery. Corticosteroids have shown some favorable outcomes in patients with SARS and COVID-19 but delayed viral clearance and secondary infections have been reported. Currently it is difficult to formulate clear recommendations regarding steroid use in COVID-19 but can be used in selected patients.

Keywords: SARS coV; SARS co V-2; Corticosteroids

×

References

  1. Wang C., et al. “A novel coronavirus outbreak of global health concern”. Lancet10223 (2020): 470-473.
  2. Shi H., et al. “Radiological findings from 81 patients with COVID-19 pneumonia in Wuhan, China: a descriptive study”. Lancet Infection Disease (2020).
  3. Chang D., et al. “Epidemiologic and Clinical Characteristics of Novel Coronavirus Infections Involving 13 Patients Outside Wuhan, China”. American Medical Association 323.11 (2020): 1092-1093.
  4. Drosten C., et al. “Identification of a novel coronavirus in patients with severe acute respiratory syndrome”. New England Journal of Medicine20 (2003): 1967-1976.
  5. Zaki AM., et al. “Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia”. New England Journal of Medicine19 (2012): 1814-1820.
  6. Cheng VCC., et al. “Severe acute respiratory syndrome coronavirus as an agent of emerging and reemerging infection”. Clinical Microbiology Review4 (2007): 660-694.
  7. Chan JF-W., et al. “Genomic characterization of the 2019 novel human-pathogenic coronavirus isolated from a patient with atypical pneumonia after visiting Wuhan”. Emerging Microbes and Infections1 (2020): 221-236.
  8. de Groot RJ., et al. “Middle East respiratory syndrome coronavirus (MERS-CoV): announcement of the Coronavirus Study Group”. Journal of Virology. American Society for Microbiology Journals14 (2013): 7790-7792.
  9. Magazine R., et al. “Prescribing Patterns of Drugs in Acute Respiratory Distress Syndrome (ARDS): An Observational Study”. Journal of Clinical and Diagnostic Research 2 (2015): FC01-04.
  10. Wang H., et al. “Fatal aspergillosis in a patient with SARS who was treated with corticosteroids”. New England Journal of Medicine5 (2003): 507-508.
  11. Stockman LJ., et al. “SARS: systematic review of treatment effects”. Low D, editor. PLoS Medicine Public Library of Science 3.9 (2006): e343.
  12. Marik PE., et al. “Recommendations for the diagnosis and management of corticosteroid insufficiency in critically ill adult patients: consensus statements from an international task force by the American College of Critical Care Medicine”. Critical Care Medicine (2008): 1937-1949.
  13. Lansbury LE., et al. “Corticosteroids as Adjunctive Therapy in the Treatment of Influenza: An Updated Cochrane Systematic Review and Meta-analysis”. Critical Care Medicine2 (2020): e98-e106.
  14. Delaney JW., et al. “The influence of corticosteroid treatment on the outcome of influenza A (H1N1pdm09)-related critical illness”. Critical Care BioMed Central1 (2016): 75-11.
  15. Russell CD., et al. “Clinical evidence does not support corticosteroid treatment for 2019-nCoV lung injury”. Lancet10223 (2020): 473-475.
  16. Bandara SMR and Herath HMMTB. “Effectiveness of corticosteroid in the treatment of dengue - A systemic review”. Elsevier 4.9 (2018): e00816.
  17. Jin Y., et al. “Virology, Epidemiology, Pathogenesis, and Control of COVID-19”. Multidisciplinary Digital Publishing Institute 12.4 (2020): 372.
  18. Gu J and Korteweg C. “Pathology and pathogenesis of severe acute respiratory syndrome”. American Journal of Pathology4 (2017): 1136-1147.
  19. Li W., et al. “Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus”. Nature Publishing Group 426.6965 (2003): 450-454.
  20. Sims AC., et al. “Severe acute respiratory syndrome coronavirus infection of human ciliated airway epithelia: role of ciliated cells in viral spread in the conducting airways of the lungs”. Journal of Virology. American Society for Microbiology Journals24 (2005): 15511-15524.
  21. Hamming I., et al. “Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis”. Journal of Pathology John Wiley and Sons, Ltd 203.2 (2004): 631-637.
  22. Yoshikawa T., et al. “Severe acute respiratory syndrome (SARS) coronavirus-induced lung epithelial cytokines exacerbate SARS pathogenesis by modulating intrinsic functions of monocyte-derived macrophages and dendritic cells”. Journal of Virology7 (2009): 3039-3048.
  23. Jeffers SA., et al. “CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus”. Proceedings of the National Academy of Sciences of the United States of America. National Academy of Sciences 101.44 (2004): 15748-15753.
  24. Marzi A., et al. “DC-SIGN and DC-SIGNR interact with the glycoprotein of Marburg virus and the S protein of severe acute respiratory syndrome coronavirus”. Journal of Virology. American Society for Microbiology Journals21 (2004): 12090-12095.
  25. Boonnak K., et al. “Role of Dendritic Cells in Antibody-Dependent Enhancement of Dengue Virus Infection”. Journal of Virology. American Society for Microbiology Journals8 (2008): 3939-3951.
  26. Pokidysheva E., et al. “Cryo-EM Reconstruction of Dengue Virus in Complex with the Carbohydrate Recognition Domain of DC-SIGN”. Cell Press 124.3 (2006): 485-493.
  27. Kuba K., et al. “A crucial role of angiotensin converting enzyme 2 (ACE2) in SARS coronavirus-induced lung injury”. Nature Medicine. Nature Publishing Group 11.8 (2005): 875-879.
  28. Nicholls JM., et al. “Lung pathology of fatal severe acute respiratory syndrome”. The Lancet9371 (2004): 1773-1778.
  29. Cheung OY., et al. “The spectrum of pathological changes in severe acute respiratory syndrome (SARS)”. 3rd ed. John Wiley and Sons, Ltd 45.2 (2004): 119-124.
  30. Ding Y., et al. “The clinical pathology of severe acute respiratory syndrome (SARS): a report from China”. Journal of Pathology John Wiley and Sons, Ltd 200.3 (2003): 282-289.
  31. Chan WS., et al. “Coronaviral hypothetical and structural proteins were found in the intestinal surface enterocytes and pneumocytes of severe acute respiratory syndrome (SARS)”. Modern Pathology Nature Publishing Group 18.11 (2005): 1432-1439.
  32. Zhang L., et al. “Antibody responses against SARS coronavirus are correlated with disease outcome of infected individuals”. Journal of Medical Virology John Wiley and Sons, Ltd 78.1 (2006): 1-8.
  33. Liu L., et al. “Anti-spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection”. JCI Insight. American Society for Clinical Investigation4 (2019): S6.
  34. Lin YS., et al. “Antibody to severe acute respiratory syndrome (SARS)‐associated coronavirus spike protein domain 2 cross‐reacts with lung epithelial cells and causes cytotoxicity”. Clinical and Experimental Immunology John Wiley and Sons, Ltd 141.3 (2005): 500-508.
  35. Yang YH., et al. “Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection”. Journal of Medical Virology. John Wiley and Sons, Ltd 77.1 (2005): 1-7.
  36. Wong CK., et al. “Plasma inflammatory cytokines and chemokines in severe acute respiratory syndrome”. Clinical and Experimental Immunology. John Wiley and Sons, Ltd 136.1 (2004): 95-103.
  37. Mahallawi WH., et al. “MERS-CoV infection in humans is associated with a pro-inflammatory Th1 and Th17 cytokine profile”. Academic Press 104 (2018): 8-13.
  38. “Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China”. The Lancet Elsevier 395.10223 (2020): 497-506.
  39. Liberman AC., et al. “Glucocorticoids in the regulation of transcription factors that control cytokine synthesis”. Cytokine and Growth Factor Reviews 18 (2020): 45-56.
  40. Liberman AC., et al. “Regulatory and Mechanistic Actions of Glucocorticoids on T and Inflammatory Cells”. Frontiers in Endocrinology (Lausanne). Frontiers 9 (2018): 235.
  41. Wandinger KP., et al. “Effect of high‐dose methylprednisolone administration on immune functions in multiple sclerosis patients”. Acta Neurologica Scandinavica. John Wiley and Sons, Ltd 97.6 (1998): 359-365.
  42. Crockard AD., et al. “Transient immunomodulation by intravenous methylprednisolone treatment of multiple sclerosis”. Multiple Sclerosis1 (1995): 20-24.
  43. Hodge Flower Han. “Methyl-Prednisolone Up-Regulates Monocyte Interleukin-10 Production in Stimulated Whole Blood”. Scandinavian Journal of Immunology. Wiley/Blackwell (10.1111) 49.5 (1999): 548-553.
  44. Moore KW., et al. “Interleukin-10 and the Interleukin-10 Receptor”. Annual Reviews 4139 El Camino Way, P.O. Box 10139, Palo Alto, CA 94303-0139, USA 19.1 (2003): 683-765.
  45. Hart KA., et al. “Effects of Low-Dose Hydrocortisone Therapy on Immune Function in Neonatal Horses”. Pediatric Research. Nature Publishing Group 70.1 (2011): 72-77.
  46. Bandara SMR and Herath HMMTB. “Corticosteroid actions on dengue immune pathology A review article”. Clinical Epidemiology and Global Health. Elsevier (2019).
  47. Barnes PJ. “How corticosteroids control inflammation: Quintiles Prize Lecture 2005”. British Journal of Pharmacology. John Wiley and Sons, Ltd 148.3 (2016): 245-254.
  48. Silwal P., et al. “Dexamethasone Induces FcγRIIb Expression in RBL-2H3 Cells”. Korean Journal of Physiology and Pharmacology 6 (2012): 393-398.
  49. Guilliams M., et al. “The function of Fcγ receptors in dendritic cells and macrophages”. Nature Reviews Immunology. Nature Publishing Group 14.2 (2014): 94-108.
  50. Nielsen DG. “The relationship of interacting immunological components in dengue pathogenesis”. Virology Journal. BioMed Central 6.1 (2009): 211.
  51. Peng Q., et al. “The role of anaphylatoxins C3a and C5a in regulating innate and adaptive immune responses”. Inflammation Allergy and Drug Targets3 (2009): 236-246.
  52. Gorski JP., et al. “C4a: the third anaphylatoxin of the human complement system”. Proceedings of the National Academy of Sciences of the United States of America 10 (1979): 5299-302.
  53. Stoermer KA and Morrison TE. “Complement and viral pathogenesis”. Virology2 (2011): 362-373.
  54. Gralinski LE., et al. “Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis”. Subbarao K, editor. mBio5 (2018): 1666.
  55. Weiler JM and Packard BD. “Methylprednisolone inhibits the alternative and amplification pathways of complement. Infection and Immunity”. American Society for Microbiology Journals1 (1982): 122-126.
  56. Hammerschmidt DE., et al. “Corticosteroids inhibit complement-induced granulocyte aggregation. A possible mechanism for their efficacy in shock states”. Journal of Clinical Investigation. American Society for Clinical Investigation 4 (1979): 798-803.
  57. Tseng C-TK., et al. “Severe acute respiratory syndrome and the innate immune responses: modulation of effector cell function without productive infection”. Journal of Immunology. American Association of Immunologists 12 (2005): 7977-7985.
  58. Jaume M., et al. “Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH- and cysteine protease-independent FcγR pathway”. Journal of Virology. American Society for Microbiology Journals 20 (2011): 10582-10597.
  59. Wan Y., et al. “Molecular Mechanism for Antibody-Dependent Enhancement of Coronavirus Entry”. Journal of Virology5 (2020).
  60. Delelis O., et al. “Integrase and integration: biochemical activities of HIV-1 integrase”. Retrovirology 1 (2008): 114.
  61. Moser M., et al. “Glucocorticoids down-regulate dendritic cell function in vitro and in vivo”. European Journal of Immunology. John Wiley and Sons, Ltd 25.10 (1995): 2818-2824.
  62. Ding Y., et al. “Organ distribution of severe acute respiratory syndrome (SARS) associated coronavirus (SARS-CoV) in SARS patients: implications for pathogenesis and virus transmission pathways”. Journal of Pathology. John Wiley and Sons, Ltd 203.2 (2004): 622-630.
  63. Hwang DM., et al. “Pulmonary pathology of severe acute respiratory syndrome in Toronto”. Modern Pathology. Nature Publishing Group 18.1 (2005): 1-10.
  64. Lee Y-R., et al. “MCP-1, a highly expressed chemokine in dengue haemorrhagic fever/dengue shock syndrome patients, may cause permeability change, possibly through reduced tight junctions of vascular endothelium cells”. Journal of Genetic Virology 87 (2006): 3623-3630.
  65. Raaben M., et al. “Cyclooxygenase activity is important for efficient replication of mouse hepatitis virus at an early stage of infection”. Virology Journal. BioMed Central1 (2007): 55-65.
  66. Steer SA and Corbett JA. “The Role and Regulation of COX-2 during Viral Infection”. 16.4 (2004): 447-460.
  67. Sander WJ, ., et al. “Prostaglandin E2 As a Modulator of Viral Infections”. Frontiers in Physiology 8 (2017): 89.
  68. Lin C-K., et al. “Cyclooxygenase‐2 facilitates dengue virus replication and serves as a potential target for developing antiviral agents”. Scientific Reports. Nature Publishing Group 7.1 (2017): 299.
  69. Lee C-H., et al. “Altered p38 mitogen-activated protein kinase expression in different leukocytes with increment of immunosuppressive mediators in patients with severe acute respiratory syndrome”. Journal of Immunology 12 (2004): 7841-7847.
  70. Liu M., et al. “Amino acids 1 to 422 of the spike protein of SARS associated coronavirus are required for induction of cyclooxygenase-2”. Virus Genes3 (2006): 309-317.
  71. Santini G., et al. “The human pharmacology of monocyte cyclooxygenase 2 inhibition by cortisol and synthetic glucocorticoids”. Clinical Pharmacology and Therapeutics. John Wiley and Sons, Ltd 70.5 (2001): 475-483.
  72. Lee N., et al. “Effects of early corticosteroid treatment on plasma SARS-associated Coronavirus RNA concentrations in adult patients”. Journal of Clinical Virology4 (2004): 304-309.
  73. Menou A., et al. “Human airway trypsin-like protease exerts potent, antifibrotic action in pulmonary fibrosis”. FASEB Journal3 (2018): 1250-1264.
  74. Yang Y., et al. “Bcl-xL inhibits T-cell apoptosis induced by expression of SARS coronavirus E protein in the absence of growth factors”. Biochemical Journal 392 (2005): 135-143.
  75. Tan Y-J., et al. “Overexpression of 7a, a protein specifically encoded by the severe acute respiratory syndrome coronavirus, induces apoptosis via a caspase-dependent pathway”. Journal of Virology. American Society for Microbiology Journal24 (2004): 14043-14047.
  76. Xu J., et al. “Orchitis: a complication of severe acute respiratory syndrome (SARS)”. Biological Reproduction2 (2006): 410-416.
  77. Chau T-N., et al. “SARS-associated viral hepatitis caused by a novel coronavirus: report of three cases”. Hepatology 2 (2004): 302-310.
  78. Hagimoto N., et al. “TGF-beta 1 as an enhancer of Fas-mediated apoptosis of lung epithelial cells”. Journal of American Association of Immunologists 168.12 (2002): 6470-6478.
  79. Meßmer UK., et al. “Suppression of apoptosis by glucocorticoids in glomerular endothelial cells: effects on proapoptotic pathways”. British Journal of Pharmacology. Wiley/Blackwell (10.1111) 129.8 (2000): 1673-1683.
  80. Radomski MW., et al. “Glucocorticoids inhibit the expression of an inducible, but not the constitutive, nitric oxide synthase in vascular endothelial cells”. Proceedings of the National Academy of Sciences of the United States of America 24 (1990): 10043-10047.
  81. Quiros M., et al. “Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling”. Journal of Clinical Investigation. American Society for Clinical Investigation9 (2017): 3510-3520.
  82. Tabardel Y., et al. “Corticosteroids increase blood interleukin-10 levels during cardiopulmonary bypass in men”. Surgery1 (1996): 76-80.
  83. Meduri GU., et al. “Effect of prolonged methylprednisolone therapy in unresolving acute respiratory distress syndrome: a randomized controlled trial”. JAMA 2 (1998): 159-165.
  84. Bernard GR., et al. “High-Dose Corticosteroids in Patients with the Adult Respiratory Distress Syndrome”. Massachusetts Medical Society25 (2010): 1565-1570.
  85. Singh A., et al. “Role of Corticosteroids Use in Ards: Comparison of Systematic Review and Meta-Analysis”. Value Health7 (2014): A726.
  86. Horita N., et al. “Impact of Corticosteroids on Mortality in Patients with Acute Respiratory Distress Syndrome: A Systematic Review and Meta-analysis”. Intern Medicine. The Japanese Society of Internal Medicine12 (2005): 1473-1479.
  87. Lee N., et al. “A Major Outbreak of Severe Acute Respiratory Syndrome in Hong Kong”. New England Journal of Medicine20 (2003): 1986-1994.
  88. Ho JC., et al. “High-dose pulse versus nonpulse corticosteroid regimens in severe acute respiratory syndrome”. American Journal of Respiratory and Critical Care Medicine12 (2003): 1449-1456.
  89. Lew TWK., et al. “Acute Respiratory Distress Syndrome in Critically Ill Patients With Severe Acute Respiratory Syndrome”. American Medical Association 290.3 (2003): 374-380.
  90. Zhao Z. “Description and clinical treatment of an early outbreak of severe acute respiratory syndrome (SARS) in Guangzhou, PR China”. Journal of Medical Microbiology. Microbiology Society8 (2003): 715-720.
  91. Fowler RA. “Critically Ill Patients With Severe Acute Respiratory Syndrome”. American Medical Association 290.3 (2003): 367.
  92. Booth CM., et al. “Clinical Features and Short-term Outcomes of 144 Patients With SARS in the Greater Toronto Area”. American Medical Association 289.21 (2003): 2801-2809.
  93. Arabi YM., et al. “Corticosteroid Therapy for Critically Ill Patients with Middle East Respiratory Syndrome. American Journal of Respiratory and Critical Care Medicine”. American Thoracic Society6 (2018): 757-767.
  94. Wang Y., et al. “Early, low-dose and short-term application of corticosteroid treatment in patients with severe COVID-19 pneumonia: single-center experience from Wuhan, China”. Cold Spring Harbor Laboratory Press (2020).
  95. Zhou Z-G., et al. “Short-Term Moderate-Dose Corticosteroid Plus Immunoglobulin Effectively Reverses COVID-19 Patients Who Have Failed Low-Dose Therapy”. Preprints (2020).
  96. Shang J., et al. “The Treatment and Outcomes of Patients with COVID-19 in Hubei, China: A Multi-Centered, Retrospective, Observational Study”. SSRN Journal (2020).
  97. Qi D., et al. “Epidemiological and clinical features of 2019-nCoV acute respiratory disease cases in Chongqing municipality, China: a retrospective, descriptive, multiple-center”. medRxiv (2020).
  98. Matsuyama S., et al. “The inhaled corticosteroid ciclesonide blocks coronavirus RNA replication by targeting viral NSP15”. Cold Spring Harbor Laboratory (2020).
  99. Mo P., et al. “Clinical characteristics of refractory COVID-19 pneumonia in Wuhan, China”. Clinical Infection Disease (2020).
×

Citation

Citation: SM Rathnasiri Bandara and HMMTB Herath. “Corticosteroid Actions on COVID-19 and SARS Viral Immune Pathology; A Review Article". Acta Scientific Microbiology 4.3 (2020): 176-190.




Metrics

Acceptance rate30%
Acceptance to publication20-30 days
Impact Factor1.172

Indexed In






News and Events


  • Certification for Review
    Acta Scientific certifies the Editors/reviewers for their review done towards the assigned articles of the respective journals.
  • Submission Timeline for Upcoming Issue
    The last date for submission of articles for regular Issues is April 25, 2021.
  • Publication Certificate
    Authors will be issued a "Publication Certificate" as a mark of appreciation for publishing their work.
  • Best Article of the Issue
    The Editors will elect one Best Article after each issue release. The authors of this article will be provided with a certificate of “Best Article of the Issue”.
  • Welcoming Article Submission
    Acta Scientific delightfully welcomes active researchers for submission of articles towards the upcoming issue of respective journals.
  • Contact US