The role of viruses in the development of autoimmune diseases
Authors:
R. Moravcová
Authors place of work:
Revmatologický ústav Praha
Published in the journal:
Čes. Revmatol., 28, 2020, No. 3, p. 160-168.
Category:
Review Article
Summary
Autoimmune diseases affect an increasing percentage of our population and are the third leading cause of morbidity and mortality in developed countries, after cardiovascular diseases and cancer. Currently, more than 80 identified autoimmune diseases are known, which represent a significant clinical problem due to their chronicity, which requires long-term and often lifelong therapy. Current therapies seek to suppress the symptoms of these diseases but have difficulty targeting the true causes of these diseases and addressing them effectively and without further side effects. At the same time, the identification of the trigger of the autoimmune disease and its removal could ensure the cure of the patient. The problem is that the exact etiology of most autoimmune diseases is not fully known. However, in addition to the genetic profile, the lifestyle of an individual with environmental triggers, such as bacterial, fungal, parasitic, and viral infections, are probably involved. And it is the viruses that have been shown to influence the development of the clinical picture of a number of autoimmune diseases, whether rheumatological, such as systemic lupus erythematosus, rheumatoid arthritis, Sjögren’s syndrome, and many others, as well as non-rheumatic conditions including type 1 diabetes, celiac disease, autoimmune thyroiditis, and multiple sclerosis. Viral infections elicit a strong immune response, which is necessary to suppress the infection. However, in some cases, failure to regulate this immune response can lead to deleterious immune responses directed against host antigens. This article focuses on the role of the most common and well-known viruses and the mechanism by which they interact with the infected host's immune system, eliciting inflammatory responses that potentially lead to the development or exacerbation of rheumatic autoimmune diseases.
Keywords:
autoimmunity – autoimmune diseases – viruses – viral infection
Zdroje
1. Kim B, Kaistha SD, Rouse BT. Viruses and autoimmunity. Autoimmunity 2006; 39(1): 71–77.
2. Fujinami RS, von Herrath MG, Christen U, et al. Molecular mimicry, bystander activation, or viral persistence: infections and autoimmune disease. Clin Microbiol Rev 2006; 19(1): 80–94.
3. Getts DR, Chastain EM, Terry RL, et al. Virus infection, antiviral immunity, and autoimmunity. Immunol Rev 2013; 255(1): 197–209.
4. Roubalová K. Laboratorní diagnostika herpetických virů. Med praxi 2010; 7(5): 241–244.
5. Poole BD, Templeton AK, Guthridge JM, et al. Aberrant Epstein-Barr viral infection in systemic lupus erythematosus. Autoimmun Rev 2009; 8(4): 337–342.
6. James JA, Neas BR, Moser KL, et al. Systemic lupus erythematosus in adults is associated with previous Epstein-Barr virus exposure. Arthritis Rheum 2001; 44(5): 1122–1126.
7. Draborg AH, Duus K, Houen G. Epstein-Barr virus and systemic lupus erythematosus. Clin Dev Immunol 2012; 2012: 370516.
8. Larsen M, Sauce D, Deback C, et al. Exhausted cytotoxic control of Epstein-Barr virus in human lupus. PLoS Pathog 2011; 7(10): e1002328.
9. Blaschke S, Schwarz G, Moneke D, et al. Epstein-Barr virus infection in peripheral blood mononuclear cells, synovial fluid cells, and synovial membranes of patients with rheumatoid arthritis. J Rheumatol 2000; 27(4): 866–873.
10. Balandraud N, Meynard JB, Auger I, et al. Epstein-Barr virus load in the peripheral blood of patients with rheumatoid arthritis: Accurate quantification using real-time polymerase chain reaction. Arthritis Rheum 2003; 48(5): 1223–1228.
11. Croia C, Serafini B, Bombardieri M, et al. Epstein-Barr virus persistence and infection of autoreactive plasma cells in synovial lymphoid structures in rheumatoid arthritis. Ann Rheum Dis 2013; 72(9): 1559–1568.
12. Klatt T, Ouyang Q, Flad T, et al. Expansion of peripheral CD8+ CD28– T cells in response to Epstein-Barr virus in patients with rheumatoid arthritis. J Rheumatol 2005; 32(2): 239–251.
13. Toussirot E, Wendling D, Tiberghien P, et al. Decreased T cell precursor frequencies to Epstein-Barr virus glycoprotein Gp110 in peripheral blood correlate with disease activity and severity in patients with rheumatoid arthritis. Ann Rheum Dis 2000; 59(7): 533–538.
14. Pasoto SG, Natalino RR, Chakkour HP, et al. EBV reactivation serological profile in primary Sjögren’s syndrome: an underlying trigger of active articular involvement? Rheumatol Int 2013; 33(5): 1149–1157.
15. Mariette X, Gozlan J, Clerc D, et al. Detection of Epstein-Barr virus DNA by in situ hybridization and polymerase chain reaction in salivary gland biopsy specimens from patients with Sjögren’s syndrome. Am J Med 1991; 90(3): 286–294.
16. Toda I, Ono M, Fujishima H, et al. Sjögren’s syndrome (SS) and Epstein-Barr virus (EBV) reactivation. Ocul Immunol Inflamm 1994; 2(2): 101–109.
17. Rahal EA, Hajjar H, Rajeh M, et al. Epstein-Barr virus and human herpes virus 6 type A DNA Enhance IL-17 Production in Mice. Viral Immunol 2015; 28(5): 297–302.
18. Salloum N, Hussein HM, Jammaz R, et al. Epstein-Barr virus DNA modulates regulatory T-cell programming in addition to enhancing interleukin-17A production via Toll-like receptor 9. PLoS One 2018; 13(7): e0200546.
19. Tabarkiewicz J, Pogoda K, Karczmarczyk A, et al. The role of IL-17 and Th17 lymphocytes in autoimmune diseases. Arch Immunol Ther Exp (Warsz) 2015; 63(6): 435–449.
20. Harley JB, Chen X, Pujato M, et al. Transcription factors operate across disease loci, with EBNA2 implicated in autoimmunity. Nat Genet 2018; 50(5): 699–707.
21. Pietiläinen J, Virtanen JO, Uotila L, et al. HHV-6 infection in multiple sclerosis. A clinical and laboratory analysis. Eur J Neurol 2010; 17(3): 506–509.
22. Challoner PB, Smith KT, Parker JD, et al. Plaque-associated expression of human herpesvirus 6 in multiple sclerosis. Proc Natl Acad Sci USA 1995; 92(16): 7440–7444.
23. Broccolo F, Drago F, Paolino S, et al. Reactivation of human herpesvirus 6 (HHV-6) infection in patients with connective tissue diseases. J Clin Virol 2009; 46(1): 43–46.
24. Broccolo F, Drago F, Cassina G, et al. Selective reactivation of human herpesvirus 6 in patients with autoimmune connective tissue diseases. J Med Virol 2013; 85(11): 1925–1934.
25. Scotet E, Peyrat MA, Saulquin X, et al. Frequent enrichment for CD8 T cells reactive against common herpes viruses in chronic inflammatory lesions: towards a reassessment of the physiopathological significance of T cell clonal expansions found in autoimmune inflammatory processes. Eur J Immunol 1999; 29(3): 973–985.
26. Schottstedt V, Blümel J, Burger R, et al. Human cytomegalovirus (HCMV) – revised. Transfus Med Hemother 2010; 37(6): 365–375.
27. Pandey JP. Immunoglobulin GM genes and IgG antibodies to cytomegalovirus in patients with systemic sclerosis. Clin Exp Rheumatol 2004; 22(3, Suppl 33): S35–37.
28. Namboodiri AM, Rocca KM, Pandey JP. IgG antibodies to human cytomegalovirus late protein UL94 in patients with systemic sclerosis. Autoimmunity 2004; 37(3): 241–244.
29. Halenius A, Hengel H. Human cytomegalovirus and autoimmune disease. Biomed Res Int 2014; 2014: 472978.
30. Palafox Sánchez CA, Satoh M, Chan EK, et al. Reduced IgG anti-small nuclear ribonucleoprotein autoantibody production in systemic lupus erythematosus patients with positive IgM anti-cytomegalovirus antibodies. Arthritis Res Ther 2009; 11(1): R27.
31. Huang MJ, Tsai SL, Huang BY, et al. Prevalence and significance of thyroid autoantibodies in patients with chronic hepatitis C virus infection: a prospective controlled study. Clin Endocrinol (Oxf) 1999; 50(4): 503–509.
32. Carrozzo M. Oral diseases associated with hepatitis C virus infection. Part 1. Sialadenitis and salivary glands lymphoma. Oral Dis 2008; 14(2): 123–130.
33. Yeh CC, Wang WC, Wu CS, et al. Association of Sjögrens syndrome in patients with chronic hepatitis virus infection: a population-based analysis. PLoS One 2016; 11(8): e0161958.
34. Aktas GE, Sarikaya A, Kandemir O. Hepatitis C virus-related arthritis: bone scintigraphic appearances. Indian J Nucl Med 2017; 32(1): 30–32.
35. Ferri C, Sebastiani M, Giuggioli D, et al. Mixed cryoglobulinemia: demographic, clinical, and serologic faetures and survival in 231 patients. Semin Arthritis Rheum 2004; 33(6): 355–374.
36. Lobigs M, Blanden RV, Müllbacher A. Flavivirus-induced up-regulation of MHC class I antigens; implications for the induction of CD8+ T-cell-mediated autoimmunity. Immunol Rev 1996; 152: 5–19.
37. Bao S, King NJ, Dos Remedios CG. Flavivirus induces MHC antigen on human myoblasts: a model of autoimmune myositis? Muscle Nerve 1992; 15(11): 1271–1277.
38. Talib SH, Bhattu S, Bhattu R. Dengue fever triggering systemic lupus erythematosus and lupus nephritis: a case report. Int Med Case Rep J 2013; 6: 71–75.
39. Fuzii HT, da Silva Dias GA, de Barros RJ, et al. Immunopathogenesis of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Life Sci 2014; 104(1–2): 9–14.
40. Brzustewicz E, Bryl E. The role of cytokines in the pathogenesis of rheumatoid arthritis – practical and potential application of cytokines as biomarkers and targets of personalized therapy. Cytokine 2015; 76(2): 527–536.
41. Nishioka K, Nakajima T, Hasunuma T, et al. Rheumatic manifestation of human leukemia virus infection. Rheum Dis Clin North Am 1993; 19(2): 489–503.
42. Nakamura H, Takahashi Y, Yamamoto-Fukuda T, et al. Direct infection of primary salivary gland epithelial cells by human T lymphotropic virus type I in patients with Sjögren’s syndrome. Arthritis Rheumatol 2015; 67(4): 1096–1106.
43. Vega LE, Espinoza LR. Human immunodeficiency virus infection (HIV)-associated rheumatic manifestations in the pre- and post-HAART eras. Clin Rheumatol 2020; 15: 1–8.
44. Yeung WC, Rawlinson WD, Craig ME. Enterovirus infection and type 1 diabetes mellitus: systematic review and meta-analysis of observational molecular studies. BMJ 2011; 342: d35.
45. Lunardi C, Tinazzi E, Bason C, et al. Human parvovirus B19 infection and autoimmunity. Autoimmun Rev 2008; 8(2): 116–120.
46. Hollinger FB, Sharp JT, Lidsky MD, et al. Antibodies to viral antigens in systemic lupus erythematosus. Arthritis Rheum 1971; 14(1): 1–11.
47. Altman A, Szyper-Kravitz M, Agmon-Levin N, et al. Prevalence of rubella serum antibody in autoimmune diseases. Rev Bras Reumatol 2012; 52(3): 307–318.
48. Poo YS, Rudd PA, Gardner J, et al. Multiple immune factors are involved in controlling acute and chronic chikungunya virus infection. PLoS Negl Trop Dis 2014; 8(12): e3354.
49. Chang AY, Martins KAO, Encinales L, et al. Chikungunya arthritis mechanisms in the americas: a cross-sectional analysis of chikungunya arthritis patients twenty-two months after infection demonstrating no detectable viral persistence in synovial fluid. Arthritis Rheumatol 2018; 70(4): 585–593.
50. McCarthy MK, Morrison TE. Persistent RNA virus infections: do PAMPS drive chronic disease? Curr Opin Virol 2017; 23: 8–15.
51. Amaral JK, Taylor PC, Teixeira MM, et al. The clinical features, pathogenesis and methotrexate therapy of chronic chikungunya arthritis. Viruses 2019; 11(3).
52. Martín-López M, Albert E, Fernández-Ruiz M, et al. Torque teno virus viremia in patients with chronic arthritis: Influence of biologic therapies. Semin Arthritis Rheum 2020; 50(1): 166–171.
53. Gergely P Jr, Perl A, Poór G. Possible pathogenic nature of the recently discovered TT virus: does it play a role in autoimmune rheumatic diseases? Autoimmun Rev 2006; 6(1): 5–9.
54. Liu Z, Xiao X, Wei X, et al. Composition and divergence of coronavirus spike proteins and host ACE2 receptors predict potential intermediate hosts of SARS-CoV-2. J Med Virol 2020; doi:10.1002/jmv.25726
55. World Health Organisation. Coronavirus disease (COVID-19) technical guidance: Laboratory testing for 2019-nCoV in humans [online].
56. UpToDate: Coronavirus disease 2019 (COVID-19) [databáze]. Wolters Kluwer Health, ©2020. Poslední revize 2020-03-20 cit. 2020-03-22].
57. Li Z, Yi Y, Luo X. Development and clinical application of a rapid IgM-IgG combined antibody test for SARS-CoV-2 infection diagnosis. J Medical Virol 2020; doi:10.1002/jmv.25727
58. Broughton JP, Deng J, Yu G. Rapid detection of 2019 novel coronavirus SARS-CoV-2 using a CRISPR-based DETECTR lateral flow assay. medRxiv 2020; doi:10.1101/2020.03.06.20032334
59. Landewé RB, Machado PM, Kroon F, et al. EULAR provisional recommendations for the management of rheumatic and musculoskeletal diseases in the context of SARS-CoV-2. Ann Rheum Dis 2020; 79(7): 851–858.
60. Haberman R, Axelrad J, Chen A, et al. Covid-19 in immune-mediated inflammatory diseases – case series from New York. N Engl J Med 2020; NEJMc2009567.
61. Ahmed SF, Quadeer AA, McKay MR. Preliminary identification of potential vaccine targets for the COVID-19 coronavirus (SARS-CoV-2) based on SARS-CoV immunological studies. Viruses 2020; 3(12): 254.
62. Prompetchara E, Ketloy Ch, Palaga T. Immune responses in COVID-19 and potential vaccines: Lessons learned from SARS and MERS epidemic. Asian Pac J Allergy Immunol 2020; 38(1): 1–9.
63. Craven J. OVID-19 vaccine tracker [online]. Regulatory Affairs Professionals Society, Poslední revize 2020-03-21.
64. Lerner A, Arleevskaya M, Schmiedl A, et al. Microbes and viruses are bugging the gut in celiac disease. Are they friends or foes? Front Microbiol 2017; 8: 1392.
65. Hussein HM, Rahal EA. The role of viral infections in the development of autoimmune diseases. Crit Rev Microbiol 2019; 45(4): 394–412.
Štítky
Dermatology & STDs Paediatric rheumatology RheumatologyČlánok vyšiel v časopise
Czech Rheumatology
2020 Číslo 3
Najčítanejšie v tomto čísle
- Current impact of seronegative rheumatoid arthritis
- The role of viruses in the development of autoimmune diseases
- Validation of Czech versions of questionnaires assessing fatigue and physical acti- vity in patients with rheumatic diseases: Fatigue Impact Scale (FIS), Multidimensional Assessment of Fatigue Scale (MAF), Human Activity Profile (HAP)
- Diet in gout – should we reduce the intake of purines?