EPSTEIN-BARR VIRUS AND CYTOMEGALOVIRUS: IS THEIR ROLE IN PEMPHIGUS REALLY INCIDENTAL? A PRELIMINARY REPORT

Cover Page


Cite item

Full Text

Abstract

Background: Epstein-Barr (EBV) and cytomegaloviral (CMV) infections are among most prevalent in the population worldwide that are associated with autoimmune processes. However, conflicting data of the studies on the role of herpes viral infections in the etiology of autoimmune pemphigus does not allow for reliable recognition of these viruses as triggers in the development and course of this bullous dermatosis. Aim: To assess specific IgM and IgG antibodies to herpes virus infections in patients with autoimmune pemphigus. Materials and methods: Serum samples from 15  patients with autoimmune pemphigus were analyzed by chemoluminescent immunoassay. Results: In the serum samples of 14/15 (93.3%) patients with autoimmune pemphigus we found specific IgG antibodies to nuclear and capsid EBV proteins at the levels of 30.7 to 600 U/mL (median, 147.5 [102.62; 313.25] U/mL) and from 33.5 to 567 U/mL (median, 186 [85.95; 492.5] U/mL), respectively. Specific IgG antibodies to the EBV early protein were found only in 6.7% of cases. In all patients, there were no specific IgM antibodies to EBV capsule antigens. All patients (100%) had specific IgG anti-CMV antibodies in the range from 64.5 to 138 U/mL (median, 103.5 [94.83; 113.75] U/mL). In 30% of cases, there were specific IgM anti-CMV antibodies at titers of 11 to 12.3 U/mL (median, 5 [5; 9.5] U/mL). Conclusion: The results of the preliminary study showed that 93.3%  of autoimmune pemphigus cases have an underlying chronic infection caused by EBV and CMV. The finding of the high titers of IgG anti-EBV and anti-CMV antibodies allows to conclude that the association of these viruses with the bullous dermatosis is not just a chance. It makes further research undoubtedly necessary. Its results would draw more accurate conclusions on the role of EBV and CMV in the pathogenesis of autoimmune pemphigus and to find new perspectives in the treatment of patients with this life-threatening disease.

About the authors

N. V. Makhneva

Moscow Regional Research and Clinical Institute (MONIKI); 61/2 Shchepkina ul., Moscow, 129110, Russian Federation

Author for correspondence.
Email: makhneva@mail.ru
MD, PhD, Professor, Chair of Dermatovenereology and Dermato-oncology, Postgraduate Training Faculty Russian Federation

N. I. Syuch

Medical Educational Scientific Clinical Center named after P.V. Mandryka; 8А Bol'shaya Olen'ya ul., Moscow, 107014, Russian Federation

Email: makhneva@mail.ru
MD, PhD, Professor, Chair of Advanced Medical Therapy, Head of Laboratory Department Russian Federation

V. V. Voronova

Moscow Regional Research and Clinical Institute (MONIKI); 61/2 Shchepkina ul., Moscow, 129110, Russian Federation

Email: makhneva@mail.ru

MD, PhD Student, Chair of Dermatovenereology and Dermato-oncology, Postgraduate Training Faculty

Russian Federation

L. V. Beletskaya

Email: makhneva@mail.ru

MD, PhD, Professor

Russian Federation

References

  1. Shoenfeld Y, Rose NR. Introduction: infection and autoimmunity. In: Shoenfeld Y, Rose NR, editors. Infection and autoimmunity. Amsterdam: Elsevier; 2004. p. 613–22.
  2. Guilherme L, Kalil J. Rheumatic fever: from sore throat to autoimamune heart lesions. Int Arch Allergy Immunol. 2004;134(1):56–64. doi: 10.1159/000077915.
  3. Faé KC, Oshiro SE, Toubert A, Charron D, Kalil J, Guilherme L. How an autoimmune reaction triggered by molecular mimicry between streptococcal M protein and cardiac tissue proteins leads to heart lesions in rheumatic heart disease. J Autoimmun. 2005;24(2):101–9. doi: 10.1016/j.jaut.2005.01.007.
  4. Wucherpfennig KW. Mechanisms for the induction of autoimmunity by infectious agents. J Clin Invest. 2001;108(8):1097–104. doi: 10.1172/JCI14235.
  5. Lehmann PV, Forsthuber T, Miller A, Sercarz EE. Spreading of T-cell autoimmunity to cryptic determinants of an autoantigen. Nature. 1992;358(6382):155–7. doi: 10.1038/358155a0.
  6. Scherer MT, Ignatowicz L, Winslow GM, Kappler JW, Marrack P. Superantigens: bacterial and viral proteins that manipulate the immune system. Annu Rev Cell Biol. 1993;9:101–28. doi: 10.1146/annurev.cb.09.110193.000533.
  7. Murali-Krishna K, Altman JD, Suresh M, Sour-dive DJ, Zajac AJ, Miller JD, Slansky J, Ahmed R. Counting antigen-specific CD8 T cells: a reevaluation of bystander activation during viral infection. Immunity. 1998;8(2):177–87. doi: 10.1016/S1074-7613(00)80470-7.
  8. Ferri C, Zignego AL. Relation between infection and autoimmunity in mixed cryoglobulinemia. Curr Opin Rheumatol. 2000;12(1): 53–60.
  9. Coppieters KT, Boettler T, von Herrath M. Virus infections in type 1 diabetes. Cold Spring Harb Perspect Med. 2012;2(1):a007682. doi: 10.1101/cshperspect.a007682.
  10. Sagi L, Sherer Y, Trau H, Shoenfeld Y. Pemphigus and infectious agents. Autoimmun Rev. 2008;8(1):33–5. doi: 10.1016/j.autrev.2008.07.021.
  11. Ruocco E, Ruocco V, Lo Schiavo A, Brunet-ti G, Wolf R. Viruses and pemphigus: an intriguing never-ending story. Dermatology. 2014;229(4):310–5. doi: 10.1159/000365845.
  12. Кишкун АА. Иммунологические и серологические исследования в клинической практике. М.: МИА; 2006. 536 с.
  13. Ross SA, Novak Z, Pati S, Boppana SB. Overview of the diagnosis of cytomegalovirus infection. Infect Disord Drug Targets. 2011;11(5):466–74. doi: 10.2174/187152611797636703.

Supplementary files

Supplementary Files
Action
1. JATS XML
Download

Copyright (c) 2016 Makhneva N.V., Syuch N.I., Voronova V.V., Beletskaya L.V.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies