SIMILARITY IN IMMUNE RESPONSE BETWEEN SARS-CoV-2 INFECTION AND AUTOIMMUNE DISEASES

Elif Zeynep Öztürk; Gülşah Alyar

Derleme

SIMILARITY IN IMMUNE RESPONSE BETWEEN SARS-CoV-2 INFECTION AND AUTOIMMUNE DISEASES

Yıl 2022, Cilt: 2 Sayı: 2, 50 - 60, 06.04.2022

Elif Zeynep Öztürk Gülşah Alyar

Öz

Autoimmune diseases are characterized by persistent inflammatory reactions that lead to organ damage and dysfunction in various organs due to the presence of autoantibodies and a deregulated immune system. Disorders of the immune system are also present in COVID-19. Autoantibody production is an important feature of autoimmune diseases. However, the underlying mechanisms are complex and still not fully understood. Infectious pathogens are believed to mimic the molecular mechanisms that trigger autoimmune diseases. Viral infection can impair immunological tolerance by exposure of antigen epitopes that elicit cross-reactive antibodies. There are numerous studies showing antigenic mimicry between viral and human proteins. Epstein-Barr virus (EBV), cytomegalovirus (CMV), and human immunodeficiency virus (HIV) are viruses that inhibit these autoimmune abilities. Similarly, there are numerous studies showing the possibility that patients with SARS-CoV-2, COVID-19 will develop multiple types of autoantibodies and autoimmune diseases. Patients have a tendency to develop more than 15 different types of autoantibodies and more than 10 different autoimmune diseases. COVID-19 has been described along with other autoimmune conditions such as synthesis of various autoantibodies, Kawasaki disease, anti-phospholipid syndrome, and Guillain-Barre syndrome. Since loss of smell has been described and linked to many autoimmune conditions, it is possible that hyposmia/anosmia in COVID-19 patients is at least partially induced by autoimmune mechanisms. The main mechanisms that may contribute to the development of autoimmunity in the disease are mechanisms: SARS-CoV-2's ability to overstimulate the immune system, induce neutrophil-related cytokine responses and excessive neutrophil extracellular trap formation, and molecular similarity between the host's own components and the virus. In addition, there are potential risks of COVID-19 on new-onset autoimmune diseases such as antiphospholipid syndrome, Guillain-Barré syndrome, Kawasaki disease and others. Recognizing these autoimmune manifestations of COVID-19 is essential in order to properly deal with the ongoing pandemic and its long-term post-pandemic consequences.

Anahtar Kelimeler

COVID-19, SARS-CoV-2, Otoimmunity, COVID-19 structure, Post COVID

Kaynakça

1. Pollard C, Morran M, Nestor-Kalinoski A. The COVID-19 pandemic: a global health crisis. Physiol Genomics. 2020.
2. Domingues R, Lippi A, Setz C, et al. SARS-CoV-2, immunosenescence and inflammaging: partners in the COVID-19 crime. Aging. 2020; 12: 18778–18789.
3. Hopfer H, Herzig M, Gosert R, et al. Hunting coronavirus by transmission electron microscopy: a guide to SARS-CoV-2-associated ultrastructural pathology in COVID-19 tissues. Histopathology. 2020.
4. De P, Bhayye S, Kumar V, Roy K. In silico modeling for quick prediction of inhibitory activity against 3CL enzyme in SARS CoV diseases. J Biomol Struct Dynamics. 2020; 1–27.
5. Yu F, Xiang R, Deng X, et al. Receptor-binding domain-specific human neutralizing monoclonal antibodies against SARS-CoV and SARS-CoV-2. Signal Transduc Target Ther. 2020; 5:212.
6. Yi C, Sun X, Ye J, et al. Key residues of the receptor binding motif in the spike protein of SARS-CoV-2 that interact with ACE2 and neutralizing antibodies. Cell Mol Immunol. 2020; 17:621–630.
7. Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 2020; 181:271–280e278.
8. Bai Y, Xu Y, Wang X, et al. Advances in SARS-CoV-2: a systematic review.Eur Rev Med Pharmacol Sci. 2020; 24:9208–9215.
9. Rothan H, Byrareddy S. The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak. J Autoimmun. 2020; 109:102433.
10. Schettino M, Pellegrini L, Picascia D, et al. Clinical characteristics of COVID19 patients with gastrointestinal symptoms in Northern Italy: a single-center cohort study. Am J Gastroenterol. 2020.
11. Qian S, Hong W, Lingjie-Mao, et al. Clinical characteristics and outcomes of severe and critical patients with 2019 novel coronavirus disease (COVID-19) in Wenzhou: a retrospective study. Front Med. 2020; 7:552002.
12. Wang J, Li Q, Yin Y, et al. Excessive neutrophils and neutrophil extracellular traps in COVID-19. Front Immunol. 2020; 11:2063.
13. Esmaeilzadeh A, Elahi R. Immunobiology and immunotherapy of COVID-19: a clinically updated overview. J Cell Physiol. 2020.
14. Pascolini S, Vannini A, Deleonardi G, et al. COVID-19 and immunological dysregulation: can autoantibodies be useful? Clin Transl Sci. 2020.
15. Hejrati A, Rafiei A, Soltanshahi M, et al. Innate immune response in systemic autoimmune diseases: a potential target of therapy. Inflammopharmacology. 2020; 28:1421–1438.
16. Singh A, Thakur M, Sharma L, Chandra K. Designing a multiepitope peptide based vaccine against SARS-CoV-2. Sci Rep. 2020; 10:16219.
17. Rydyznski Moderbacher C, Ramirez S, Dan J. Antigen-specific adaptive immunity to SARS-CoV-2 in acute COVID-19 and associations with age and disease severity. Cell. 2020; 183:996–1012.e19.
18. Lancman G, Mascarenhas J, Bar-Natan M. Severe COVID-19 virus reactivation following treatment for B cell acute lymphoblastic leukemia. J Hematol Oncol. 2020; 13:131.
19. Setiati S, Harimurti K, Safitri E, et al. Risk factors and laboratory test results associated with severe illness and mortality in COVID-19 patients: a systematic review. Acta Med Indones. 2020; 52:227–245.
20. Ziadi A, Hachimi A, Admou B, et al. Lymphopenia in critically ill COVID-19 patients: a predictor factor of severity and mortality. Int J Lab Hematol. 2020.
21. Ciceri F, Castagna A, Rovere-Querini P, et al. Early predictors of clinical outcomes of COVID-19 outbreak in Milan, Italy. Clin Immunol. 2020; 217:108509.
22. Satış H, Özger H, Aysert Yıldız P. Prognostic value of interleukin-18 and its association with other inflammatory markers and disease severity in COVID-19. Cytokine. 2020; 137:155302.
23. Vassallo M, Manni S, Pini P, et al. Patients with Covid-19 exhibit different immunological profiles according to their clinical presentation. Int J Infect Dis. 2020; 101:174–179.
24. Azar M, Shin J, Kang I, Landry M. Diagnosis of SARS-CoV-2 infection in the setting of cytokine release syndrome. Expert Rev Mol Diagn. 2020.
25. Sun Y, Dong Y, Wang L, et al. Characteristics and prognostic factors of disease severity in patients with COVID-19: the Beijing experience. J Autoimmun. 2020; 112:102473.
26. Chen L, Long X, Xu Q, et al. Elevated serum levels of S100A8/A9 and HMGB1 at hospital admission are correlated with inferior clinical outcomes in COVID-19 patients. Cell Mol Immunol. 2020; 17:992–994.
27. Conti P, Caraffa A, Gallenga C, et al. Coronavirus-19 (SARS-CoV-2) induces acute severe lung inflammation via IL-1 causing cytokine storm in COVID-19: a promising inhibitory strategy. J Biol Regulat Homeost Agents. 2020; 34.
28. Wampler Muskardin T. Intravenous Anakinra for macrophage activation syndrome may hold lessons for treatment of cytokine storm in the setting of coronavirus disease 2019. ACR Open Rheumatol. 2020; 2:283–285.
29. Conti P, Caraffa A, Tete` G, et al. Mast cells activated by SARS-CoV-2 release histamine which increases IL-1 levels causing cytokine storm and inflammatory reaction in COVID-19. J Biol Regul Homeost Agents. 2020; 34:1629–1632.
30. Woodruff M, Ramonell R, Nguyen D, et al. Extrafollicular B cell responses correlate with neutralizing antibodies and morbidity in COVID-19. Nat Immunol. 2020; 21:1506–1516.
31. Oliviero B, Varchetta S, Mele D, et al. Expansion of atypical memory B cells is a prominent feature of COVID-19. Cell Mol Immunol. 2020; 17:1101–1103.
32. Varchetta S, Mele D, Oliviero B, et al. Unique immunological profile in patients with COVID-19. Cell Mol Immunol. 2020. 33. Zuo Y, Yalavarthi S, Shi H, et al. Neutrophil extracellular traps in COVID-19.JCI Insight. 2020; 5
34. Ali RA, Gandhi AA, Meng H, et al. Adenosine receptor agonism protects against NETosis and thrombosis in antiphospholipid syndrome. Nat Commun. 2019; 10:1916.
35. Kaminski M, Sunny S, Balabayova K, et al. Tocilizumab therapy of COVID-19: a comparison of subcutaneous and intravenous therapies. Int J Infect Dis. 2020.
36. Liu Y, Chang C, Lu Q. Management strategies for patients with autoimmune diseases during the COVID-19 pandemic: a perspective from China. Eur J Rheumatol. 2020; 7:S94–S96.
37. Canziani L, Trovati S, Brunetta E, et al. Interleukin-6 receptor blocking with intravenous tocilizumab in COVID-19 severe acute respiratory distress syndrome: a retrospective case-control survival analysis of 128 patients. J Autoimmunity. 2020; 114:102511.
38. Iglesias-Julia´n E, Lo´pez-Veloso M, de-la-Torre-Ferrera N, et al. High döşe subcutaneous Anakinra to treat acute respiratory distress syndrome secondary to cytokine storm syndrome among severely ill COVID-19 patients. J Autoimmun. 2020; 115:102537
39. Reyes-Castillo Z, Valde´ s-Miramontes E, Llamas-Covarrubias M, Mun˜oz-Vallem J. Troublesome friends within us: the role of gut microbiota on rheumatoid arthritis etiopathogenesis and its clinical and therapeutic relevance. Clin Exp Med. 2020.
40. Harley JB, James JA. Everyone comes from somewhere: systemic lupus erythematosus and Epstein-Barr virus induction of host interferon and humoral anti Epstein-Barr nuclear antigen 1 immunity. Arthritis Rheum. 2010; 62:1571–1575.
41. Jog NR, Young KA, Munroe ME, et al. Association of Epstein-Barr virüs serological reactivation with transitioning to systemic lupus erythematosus in at-risk individuals. Ann Rheum Dis. 2019; 78:1235–1241.
42. Jog NR, McClain MT, Heinlen LD, et al. Epstein Barr virus nuclear antigen 1 (EBNA-1) peptides recognized by adult multiple sclerosis patient sera induce neurologic symptoms in a murine model. J Autoimmun. 2020; 106:102332.
43. Ramasamy R, Mohammed F, Meier U. HLA DR2b-binding peptides from human endogenous retrovirus envelope, Epstein-Barr virus and brain proteins in the context of molecular mimicry in multiple sclerosis. Immunol Lett. 2020;217:15–24.
44. Basavalingappa R, Arumugam R, Lasrado N, et al. Viral myocarditis involves the generation of autoreactive T cells with multiple antigen specificities that localize in lymphoid and nonlymphoid organs in the mouse model of CVB3 infection. Mol Immunol. 2020; 124:218–228.
45. Anand P, Puranik A, Aravamudan M, et al. SARS-CoV-2 strategically mimics proteolytic activation of human ENaC. eLife. 2020; 9.
46. Lucchese G, Floel A. Molecular mimicry between SARS-CoV-2 and respiratory pacemaker neurons. Autoimmun Rev. 2020; 19:102556.
47. Marino Gammazza A, Le´ gare´ S, Lo Bosco G, et al. Human molecular chaperones share with SARS-CoV-2 antigenic epitopes potentially capable of eliciting autoimmunity against endothelial cells: possible role of molecular mimicry in COVID-19. Cell Stress Chaperones. 2020; 25:737–741.
48. Lucchese G, Flo¨ el A. SARS-CoV-2 and Guillain-Barre´ syndrome: molecular mimicry with human heat shock proteins as potential pathogenic mechanism. Cell Stress Chaperones. 2020; 25:731–735.
49. Venkatakrishnan A, Kayal N, Anand P, et al. Benchmarking evolutionary tinkering underlying human-viral molecular mimicry shows multiple host pulmonary-arterial peptides mimicked by SARS-CoV-2. Cell Death Discov. 2020; 6:96.
50. Kanduc D. From anti-SARS-CoV-2 immune responses to COVID-19 via molecular mimicry. Antibodies (Basel). 2020; 9.
51. Reyes Gil M, Barouqa M, Szymanski J, et al. Assessment of lupus anticoagulant positivity in patients with coronavirus disease 2019 (COVID-19). JAMA Netw Open. 2020; 3:e2017539.
52. Amezcua-Guerra L, Rojas-Velasco G, Brianza-Padilla M, et al. Presence of antiphospholipid antibodies in COVID-19: case series study. Ann Rheum Dis. 2020.
53. Pinto A, Carroll L, Nar V, et al. CNS inflammatory vasculopathy with antimyelin oligodendrocyte glycoprotein antibodies in COVID-19. Neurol Neuroimmunol Neuroinflamm. 2020; 7.
54. Guilmot A, Maldonado Slootjes S, Sellimi A, et al. Immune-mediated neurological syndromes in SARS-CoV-2-infected patients. J Neurol. 2020.
55. Jensen C, Wilson S, Thombare A, et al. Cold agglutinin syndrome as a complication of Covid-19 in two cases. Clin Infect Pract. 2020; 7:100041.
56. Fujii H, Tsuji T, Yuba T, et al. High levels of anti-SSA/Ro antibodies in COVID19 patients with severe respiratory failure: a case-based review: high levels of anti-SSA/Ro antibodies in COVID-19. Clin Rheumatol. 2020.
57. Berzuini A, Bianco C, Paccapelo C, et al. Red cell-bound antibodies and transfusion requirements in hospitalized patients with COVID-19. Blood. 2020; 136:766–768.
58. Maslov D, Simenson V, Jain S, Badari A. COVID-19 and cold agglutinin hemolytic anemia. TH Open. 2020; 4:e175–e177.
59. Patil N, Herc E, Girgis M. Cold agglutinin disease and autoimmune hemolytic anemia with pulmonary embolism as a presentation of COVID-19 infection. Hematol Oncol Stem Cell Ther. 2020.
60. Gigli G, Vogrig A, Nilo A, et al. HLA and immunological features of SARS-CoV-2-induced Guillain-Barre´ syndrome. Neurol Sci. 2020; 41:3391–3394.
61. Finsterer J, Scorza F, Fiorini A. SARS-CoV-2 associated Guillain-Barre syndrome in 62 patients. Eur J Neurol. 2020.
62. Uncini A, Vallat J, Jacobs B. Guillain-Barre´ syndrome in SARS-CoV-2 infection: an instant systematic review of the first six months of pandemic. J Neurol Neurosurg Psychiatry. 2020; 91:1105–1110.
63. Bonometti R, Sacchi M, Stobbione P, et al. The first case of systemic lupus erythematosus (SLE) triggered by COVID-19 infection. Eur Rev Med Pharmacol Sci. 2020; 24:9695–9697

Yıl 2022, Cilt: 2 Sayı: 2, 50 - 60, 06.04.2022

Elif Zeynep Öztürk Gülşah Alyar

Öz

Kaynakça

1. Pollard C, Morran M, Nestor-Kalinoski A. The COVID-19 pandemic: a global health crisis. Physiol Genomics. 2020.
2. Domingues R, Lippi A, Setz C, et al. SARS-CoV-2, immunosenescence and inflammaging: partners in the COVID-19 crime. Aging. 2020; 12: 18778–18789.
3. Hopfer H, Herzig M, Gosert R, et al. Hunting coronavirus by transmission electron microscopy: a guide to SARS-CoV-2-associated ultrastructural pathology in COVID-19 tissues. Histopathology. 2020.
4. De P, Bhayye S, Kumar V, Roy K. In silico modeling for quick prediction of inhibitory activity against 3CL enzyme in SARS CoV diseases. J Biomol Struct Dynamics. 2020; 1–27.
5. Yu F, Xiang R, Deng X, et al. Receptor-binding domain-specific human neutralizing monoclonal antibodies against SARS-CoV and SARS-CoV-2. Signal Transduc Target Ther. 2020; 5:212.
6. Yi C, Sun X, Ye J, et al. Key residues of the receptor binding motif in the spike protein of SARS-CoV-2 that interact with ACE2 and neutralizing antibodies. Cell Mol Immunol. 2020; 17:621–630.
7. Hoffmann M, Kleine-Weber H, Schroeder S, et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell. 2020; 181:271–280e278.
8. Bai Y, Xu Y, Wang X, et al. Advances in SARS-CoV-2: a systematic review.Eur Rev Med Pharmacol Sci. 2020; 24:9208–9215.
9. Rothan H, Byrareddy S. The epidemiology and pathogenesis of coronavirus disease (COVID-19) outbreak. J Autoimmun. 2020; 109:102433.
10. Schettino M, Pellegrini L, Picascia D, et al. Clinical characteristics of COVID19 patients with gastrointestinal symptoms in Northern Italy: a single-center cohort study. Am J Gastroenterol. 2020.
11. Qian S, Hong W, Lingjie-Mao, et al. Clinical characteristics and outcomes of severe and critical patients with 2019 novel coronavirus disease (COVID-19) in Wenzhou: a retrospective study. Front Med. 2020; 7:552002.
12. Wang J, Li Q, Yin Y, et al. Excessive neutrophils and neutrophil extracellular traps in COVID-19. Front Immunol. 2020; 11:2063.
13. Esmaeilzadeh A, Elahi R. Immunobiology and immunotherapy of COVID-19: a clinically updated overview. J Cell Physiol. 2020.
14. Pascolini S, Vannini A, Deleonardi G, et al. COVID-19 and immunological dysregulation: can autoantibodies be useful? Clin Transl Sci. 2020.
15. Hejrati A, Rafiei A, Soltanshahi M, et al. Innate immune response in systemic autoimmune diseases: a potential target of therapy. Inflammopharmacology. 2020; 28:1421–1438.
16. Singh A, Thakur M, Sharma L, Chandra K. Designing a multiepitope peptide based vaccine against SARS-CoV-2. Sci Rep. 2020; 10:16219.
17. Rydyznski Moderbacher C, Ramirez S, Dan J. Antigen-specific adaptive immunity to SARS-CoV-2 in acute COVID-19 and associations with age and disease severity. Cell. 2020; 183:996–1012.e19.
18. Lancman G, Mascarenhas J, Bar-Natan M. Severe COVID-19 virus reactivation following treatment for B cell acute lymphoblastic leukemia. J Hematol Oncol. 2020; 13:131.
19. Setiati S, Harimurti K, Safitri E, et al. Risk factors and laboratory test results associated with severe illness and mortality in COVID-19 patients: a systematic review. Acta Med Indones. 2020; 52:227–245.
20. Ziadi A, Hachimi A, Admou B, et al. Lymphopenia in critically ill COVID-19 patients: a predictor factor of severity and mortality. Int J Lab Hematol. 2020.
21. Ciceri F, Castagna A, Rovere-Querini P, et al. Early predictors of clinical outcomes of COVID-19 outbreak in Milan, Italy. Clin Immunol. 2020; 217:108509.
22. Satış H, Özger H, Aysert Yıldız P. Prognostic value of interleukin-18 and its association with other inflammatory markers and disease severity in COVID-19. Cytokine. 2020; 137:155302.
23. Vassallo M, Manni S, Pini P, et al. Patients with Covid-19 exhibit different immunological profiles according to their clinical presentation. Int J Infect Dis. 2020; 101:174–179.
24. Azar M, Shin J, Kang I, Landry M. Diagnosis of SARS-CoV-2 infection in the setting of cytokine release syndrome. Expert Rev Mol Diagn. 2020.
25. Sun Y, Dong Y, Wang L, et al. Characteristics and prognostic factors of disease severity in patients with COVID-19: the Beijing experience. J Autoimmun. 2020; 112:102473.
26. Chen L, Long X, Xu Q, et al. Elevated serum levels of S100A8/A9 and HMGB1 at hospital admission are correlated with inferior clinical outcomes in COVID-19 patients. Cell Mol Immunol. 2020; 17:992–994.
27. Conti P, Caraffa A, Gallenga C, et al. Coronavirus-19 (SARS-CoV-2) induces acute severe lung inflammation via IL-1 causing cytokine storm in COVID-19: a promising inhibitory strategy. J Biol Regulat Homeost Agents. 2020; 34.
28. Wampler Muskardin T. Intravenous Anakinra for macrophage activation syndrome may hold lessons for treatment of cytokine storm in the setting of coronavirus disease 2019. ACR Open Rheumatol. 2020; 2:283–285.
29. Conti P, Caraffa A, Tete` G, et al. Mast cells activated by SARS-CoV-2 release histamine which increases IL-1 levels causing cytokine storm and inflammatory reaction in COVID-19. J Biol Regul Homeost Agents. 2020; 34:1629–1632.
30. Woodruff M, Ramonell R, Nguyen D, et al. Extrafollicular B cell responses correlate with neutralizing antibodies and morbidity in COVID-19. Nat Immunol. 2020; 21:1506–1516.
31. Oliviero B, Varchetta S, Mele D, et al. Expansion of atypical memory B cells is a prominent feature of COVID-19. Cell Mol Immunol. 2020; 17:1101–1103.
32. Varchetta S, Mele D, Oliviero B, et al. Unique immunological profile in patients with COVID-19. Cell Mol Immunol. 2020. 33. Zuo Y, Yalavarthi S, Shi H, et al. Neutrophil extracellular traps in COVID-19.JCI Insight. 2020; 5
34. Ali RA, Gandhi AA, Meng H, et al. Adenosine receptor agonism protects against NETosis and thrombosis in antiphospholipid syndrome. Nat Commun. 2019; 10:1916.
35. Kaminski M, Sunny S, Balabayova K, et al. Tocilizumab therapy of COVID-19: a comparison of subcutaneous and intravenous therapies. Int J Infect Dis. 2020.
36. Liu Y, Chang C, Lu Q. Management strategies for patients with autoimmune diseases during the COVID-19 pandemic: a perspective from China. Eur J Rheumatol. 2020; 7:S94–S96.
37. Canziani L, Trovati S, Brunetta E, et al. Interleukin-6 receptor blocking with intravenous tocilizumab in COVID-19 severe acute respiratory distress syndrome: a retrospective case-control survival analysis of 128 patients. J Autoimmunity. 2020; 114:102511.
38. Iglesias-Julia´n E, Lo´pez-Veloso M, de-la-Torre-Ferrera N, et al. High döşe subcutaneous Anakinra to treat acute respiratory distress syndrome secondary to cytokine storm syndrome among severely ill COVID-19 patients. J Autoimmun. 2020; 115:102537
39. Reyes-Castillo Z, Valde´ s-Miramontes E, Llamas-Covarrubias M, Mun˜oz-Vallem J. Troublesome friends within us: the role of gut microbiota on rheumatoid arthritis etiopathogenesis and its clinical and therapeutic relevance. Clin Exp Med. 2020.
40. Harley JB, James JA. Everyone comes from somewhere: systemic lupus erythematosus and Epstein-Barr virus induction of host interferon and humoral anti Epstein-Barr nuclear antigen 1 immunity. Arthritis Rheum. 2010; 62:1571–1575.
41. Jog NR, Young KA, Munroe ME, et al. Association of Epstein-Barr virüs serological reactivation with transitioning to systemic lupus erythematosus in at-risk individuals. Ann Rheum Dis. 2019; 78:1235–1241.
42. Jog NR, McClain MT, Heinlen LD, et al. Epstein Barr virus nuclear antigen 1 (EBNA-1) peptides recognized by adult multiple sclerosis patient sera induce neurologic symptoms in a murine model. J Autoimmun. 2020; 106:102332.
43. Ramasamy R, Mohammed F, Meier U. HLA DR2b-binding peptides from human endogenous retrovirus envelope, Epstein-Barr virus and brain proteins in the context of molecular mimicry in multiple sclerosis. Immunol Lett. 2020;217:15–24.
44. Basavalingappa R, Arumugam R, Lasrado N, et al. Viral myocarditis involves the generation of autoreactive T cells with multiple antigen specificities that localize in lymphoid and nonlymphoid organs in the mouse model of CVB3 infection. Mol Immunol. 2020; 124:218–228.
45. Anand P, Puranik A, Aravamudan M, et al. SARS-CoV-2 strategically mimics proteolytic activation of human ENaC. eLife. 2020; 9.
46. Lucchese G, Floel A. Molecular mimicry between SARS-CoV-2 and respiratory pacemaker neurons. Autoimmun Rev. 2020; 19:102556.
47. Marino Gammazza A, Le´ gare´ S, Lo Bosco G, et al. Human molecular chaperones share with SARS-CoV-2 antigenic epitopes potentially capable of eliciting autoimmunity against endothelial cells: possible role of molecular mimicry in COVID-19. Cell Stress Chaperones. 2020; 25:737–741.
48. Lucchese G, Flo¨ el A. SARS-CoV-2 and Guillain-Barre´ syndrome: molecular mimicry with human heat shock proteins as potential pathogenic mechanism. Cell Stress Chaperones. 2020; 25:731–735.
49. Venkatakrishnan A, Kayal N, Anand P, et al. Benchmarking evolutionary tinkering underlying human-viral molecular mimicry shows multiple host pulmonary-arterial peptides mimicked by SARS-CoV-2. Cell Death Discov. 2020; 6:96.
50. Kanduc D. From anti-SARS-CoV-2 immune responses to COVID-19 via molecular mimicry. Antibodies (Basel). 2020; 9.
51. Reyes Gil M, Barouqa M, Szymanski J, et al. Assessment of lupus anticoagulant positivity in patients with coronavirus disease 2019 (COVID-19). JAMA Netw Open. 2020; 3:e2017539.
52. Amezcua-Guerra L, Rojas-Velasco G, Brianza-Padilla M, et al. Presence of antiphospholipid antibodies in COVID-19: case series study. Ann Rheum Dis. 2020.
53. Pinto A, Carroll L, Nar V, et al. CNS inflammatory vasculopathy with antimyelin oligodendrocyte glycoprotein antibodies in COVID-19. Neurol Neuroimmunol Neuroinflamm. 2020; 7.
54. Guilmot A, Maldonado Slootjes S, Sellimi A, et al. Immune-mediated neurological syndromes in SARS-CoV-2-infected patients. J Neurol. 2020.
55. Jensen C, Wilson S, Thombare A, et al. Cold agglutinin syndrome as a complication of Covid-19 in two cases. Clin Infect Pract. 2020; 7:100041.
56. Fujii H, Tsuji T, Yuba T, et al. High levels of anti-SSA/Ro antibodies in COVID19 patients with severe respiratory failure: a case-based review: high levels of anti-SSA/Ro antibodies in COVID-19. Clin Rheumatol. 2020.
57. Berzuini A, Bianco C, Paccapelo C, et al. Red cell-bound antibodies and transfusion requirements in hospitalized patients with COVID-19. Blood. 2020; 136:766–768.
58. Maslov D, Simenson V, Jain S, Badari A. COVID-19 and cold agglutinin hemolytic anemia. TH Open. 2020; 4:e175–e177.
59. Patil N, Herc E, Girgis M. Cold agglutinin disease and autoimmune hemolytic anemia with pulmonary embolism as a presentation of COVID-19 infection. Hematol Oncol Stem Cell Ther. 2020.
60. Gigli G, Vogrig A, Nilo A, et al. HLA and immunological features of SARS-CoV-2-induced Guillain-Barre´ syndrome. Neurol Sci. 2020; 41:3391–3394.
61. Finsterer J, Scorza F, Fiorini A. SARS-CoV-2 associated Guillain-Barre syndrome in 62 patients. Eur J Neurol. 2020.
62. Uncini A, Vallat J, Jacobs B. Guillain-Barre´ syndrome in SARS-CoV-2 infection: an instant systematic review of the first six months of pandemic. J Neurol Neurosurg Psychiatry. 2020; 91:1105–1110.
63. Bonometti R, Sacchi M, Stobbione P, et al. The first case of systemic lupus erythematosus (SLE) triggered by COVID-19 infection. Eur Rev Med Pharmacol Sci. 2020; 24:9695–9697

Toplam 62 adet kaynakça vardır.

Ayrıntılar

Birincil Dil	İngilizce
Konular	Eczacılık ve İlaç Bilimleri
Bölüm	Reviews
Yazarlar	Elif Zeynep Öztürk 0000-0002-8741-2766 Gülşah Alyar 0000-0003-3628-6664
Yayımlanma Tarihi	6 Nisan 2022
Yayımlandığı Sayı	Yıl 2022 Cilt: 2 Sayı: 2

Kaynak Göster

EndNote	Öztürk EZ, Alyar G (01 Nisan 2022) SIMILARITY IN IMMUNE RESPONSE BETWEEN SARS-CoV-2 INFECTION AND AUTOIMMUNE DISEASES. International Journal of PharmATA 2 2 50–60.

Kapak Resmi İndir

Makale Dosyaları

Tam Metin