NETWORKING BETWEEN COVID-19 AND AUTOIMMUNE DISEASES: LITERATURE REVIEW
DOI:
https://doi.org/10.47820/recima21.v3i10.2086Keywords:
Autoantibodies., COVID-19, Autoimmune disease.Abstract
Introduction: COVID-19 is an infectious disease caused by coronavirus-2 associated with severe acute respiratory syndrome (SARS-CoV-2). Although most infected individuals are asymptomatic, a proportion of patients with COVID-19 develop severe disease with multiple organ damage. Aim: The present study aimed to correlate autoimmune diseases with the mechanisms triggered by SARS-CoV-2 infection. Methodology: The Center for Biotechnology Information (PubMed) and the Scientific Electronic Library Online (SciELO) databases were used for this study. As inclusion criteria, articles arising from the correlation of autoimmune diseases with COVID-19 were selected. Development: Studies have elucidated that SARS-CoV-2 can disrupt self-tolerance and trigger immune responses through cross-reactivity with host cells, culminating in the production of autoantibodies, and consequently, the development of autoimmune diseases. However, the risk of infection and prognosis of COVID-19 in patients with autoimmune diseases remains controversial, and further studies are needed to understand the complexity of the correlation between the virus and the onset of these diseases. Conclusion: Understanding the immunological mechanisms involved is of fundamental importance, and may open new avenues for the design of effective therapies.
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ANGILERI, F., et al. Is molecular mimicry the culprit in the autoimmune haemolytic anaemia affecting patients with COVID-19?. British journal of haematology, 190(2), e92–e93, 2020.
BENUCCI, M., DAMIANI, A., INFANTINO, M., MANFREDI, M., & QUARTUCCIO, L. Old and new antirheumatic drugs for the treatment of COVID-19. Joint bone spine, 87(3), pp. 195–197, 2020.
BLANCO-MELO, et al. Imbalanced Host Response to SARS-CoV-2 Drives Development of COVID-19. Cell, 181(5), pp. 1036–1045.e9, 2020.
BRUCE, I. N. et al. Factors associated with damage accrual in patients with systemic lupus erythematosus: results from the Systemic Lupus International Collaborating Clinics (SLICC) Inception Cohort. Annals of the rheumatic diseases, 74(9), pp. 1706–1713, 2015.
CHANNAPPANAVAR, R. et al. Dysregulated Type I Interferon and Inflammatory Monocyte-Macrophage Responses Cause Lethal Pneumonia in SARS-CoV-Infected Mice. Cell host & microbe, 19(2), pp. 181–193, 2016.
CIAFFI, J., MELICONI, R., RUSCITTI, P., BERARDICURTI, O., GIACOMELLI, R., & URSINI, F. Rheumatic manifestations of COVID-19: a systematic review and meta-analysis. BMC rheumatology, 4, p. 65, 2020.
DAHM, T., RUDOLPH, H., SCHWERK, CH., SCHROTEN, H. & TENENBAUM T. Neuroinvasion and Inflammation in Viral Central Nervous System Infections. Mediators of inflammation, 2016, 8562805, 2016.
DALAKAS, M. C. Guillain-Barré syndrome: The first documented COVID-19-triggered autoimmune neurologic disease: More to come with myositis in the offing. Neurology(R) neuroimmunology & neuroinflammation, 7(5), e781, 2020.
DHORIA, V., et al. Rheumatic disease. Bull Hist Med; 14, pp. 123-6, 2020.
EHRENFELD, M., et al. Covid-19 and autoimmunity. Elsevier Public Health Emergency Collection, 19(8), 102597, 2020.
FAVA, A., & PETRI, M. Systemic Lupus Erythematosus: Diagnosis and Clinical Management. Journal of autoimmunity, 96, pp. 1-13, 2020.
FERNANDEZ-GUTIERREZ, et al. Prevalence of hospital PCR-confirmed COVID-19 cases in patients with chronic inflammatory and autoimmune rheumatic diseases. Annals of rheumatic diseases, 79(9), pp. 1170-1173, 2020.
FERNANDEZ-RUIZ, R., PAREDES, J. L., & NIEWOLD, T. B. COVID-19 in patients with systemic lupus erythematosus: lessons learned from the inflammatory disease. Translational research : the journal of laboratory and clinical medicine, 232, pp. 13–36, 2021.
GALEOTTI, C., & BAYRY, J. Autoimmune and inflammatory diseases following COVID-19. Nature reviews. Rheumatology, 16(8), 413–414, 2020.
GEHRS, B. C. & FRIEDBERG, R. C. Autoimmune hemolytic anemia. American Journal of Hematology, v. 69, pp. 258-271, 2002.
GIGLI, G. L., et al. HLA and immunological features of SARS-CoV-2-induced Guillain-Barré syndrome. Neurological sciences: official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 41(12), pp. 3391–3394, 2020.
HADJADJ, J., ET al. Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients. Science, 369(6504), pp. 718–724, 2020.
HALPERT, G., & SHOENFELD, Y. SARS-CoV-2, the autoimmune virus. Autoimmunity reviews, 19(12), p. 102695, 2020.
JACOBS, J., & EICHBAUM, Q. COVID-19 associated with severe autoimmune hemolytic anemia. Transfusion, 61(2), pp. 635–640, 2021.
JIN H, et al. Consensus for prevention and management of coronavirus disease 2019 (COVID-19) for neurologists. Stroke Vasc Neurol, 5(2), pp. 146-51, 2020.
KIRIAKIDOU, M., & CHING, C. L. Systemic Lupus Erythematosus. Annals of internal medicine, 172(11), ITC81–ITC96, 2020.
LAKOTA, K., et al. COVID-19 in Association With Development, Course, and Treatment of Systemic Autoimmune Rheumatic Diseases. Frontiers in immunology, 11, 611318, 2021.
LAZARIAN, G., et al. Autoimmune haemolytic anaemia associated with COVID-19 infection. British journal of haematology, 190(1), pp. 29–31, 2020.
LIU, Y., SAWALHA, A. H., & LU, Q. COVID-19 and autoimmune diseases. Current opinion in rheumatology, 33(2), pp. 155–162, 2021.
MARES, J., & HARTUNG, H. P. Multiple sclerosis and COVID-19. Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia, 164(3), 217–225, 2020.
MASLOV, D. V., SIMENSON, V., JAIN, S., & BADARI, A. COVID-19 and Cold Agglutinin Hemolytic Anemia. TH open: companion journal to thrombosis and haemostasis, 4(3), e175–e177, 2020.
MATUCCI-CERINIC, M., HUGHES, M., TALIANI, G., & KAHALEH, B. Similarities between COVID-19 and systemic sclerosis early vasculopathy: A "viral" challenge for future research in scleroderma. Autoimmunity reviews, 20(10), 102899, 2021.
NICHOLAS, R., & RASHID, W. Multiple sclerosis. American family physician, 87(10), 712–714, 2013.
PASCOLINI, S. et al. COVID-19 and Immunological Dysregulation: Can Autoantibodies be Useful?. Clinical and translational science, 14(2), pp. 502–508, 2021.
PICCHIANTI DIAMANTI, A., ROSADO, M. M., PIOLI, C., SESTI, G., & LAGANÀ, B. Cytokine Release Syndrome in COVID-19 Patients, A New Scenario for an Old Concern: The Fragile Balance between Infections and Autoimmunity. International journal of molecular sciences, 21(9), p. 3330, 2020.
POLLARD, C. A., MORRAN, M. P., & NESTOR-KALINOSKI, A. L. The COVID-19 pandemic: a global health crisis. Physiological genomics, 52(11), pp. 549–557, 2020.
PONTILLO, A., et al. Polimorphisms in inflammasome genes are involved in the predisposition to systemic lupus erythematosus. Autoimmunity, 45(4), pp. 271–278, 2012.
SACCHI, M. C. et al. SARS-CoV-2 infection as a trigger of autoimmune response. Clinical and translational Science, 14(3), pp. 898-907, 2021.
SHAH, S., et al. Autoimmune and rheumatic musculoskeletal diseases as a consequence of SARS-CoV-2 infection and its treatment. Rheumatology international, 40(10), pp. 1539–1554, 2020.
VALK, S. J, et al. Convalescent plasma or hyperimmune immunoglobulin for people with COVID-19: a rapid review. Cochrane Database of Systematic Reviews, 5, pp 5, 2020.
VITA, R., et al. The immune epitope database (IEDB) 3.0. Nucleic acids research, 43(Database issue), D405–D412, 2015.
WILLISON, H. J., JACOBS, B. C. & DOORN, P. A VAN. Guillain-Barré syndrome. The Lancet, 388 (10045), pp. 717-727, 2016.
ZUBERBÜHLER, P., et al. Guillain-Barre syndrome associated to COVID-19 infection: a review of published case reports. Síndrome de Guillain-Barré asociado a infección por COVID-19: revisión de casos publicados. Revista de neurologia, 72(6), 203–212, 2021.
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