ISSN 2415-3060 (print), ISSN 2522-4972 (online)
  • 19 of 41
Up
JMBS 2017, 2(5): 92–99
https://doi.org/10.26693/jmbs02.05.092
Clinical Medicine

Research of Dynamics of Immune Response Rates in Patients with EVB Infection

Liadova T., Volobueva O., Zagorodneva O., Gamilovskaya A.
Abstract

In patients with infectious mononucleosis (MI) (n=30), chronic EVB infection (HEVB) (n = 30), and 20 patients in the control group, the nature and complex state of the subpopulations of immune response cells was studied. During the research all norms of international and Ukrainian protocols were observed. Clinical examination of patients with EVB and healthy patients included examination of complaints, epidemiological anamnesis, anamnesis of the disease and life, objective examination, standard instrumental and laboratory studies in dynamics, detection of replicative activity of EVB DNA and complex analysis of the immune response. The main subpopulations of peripheral blood lymphocytes (CD3+, CD4+, CD8+, CD16+, CD20+, CD25+) were determined using a set of monoclonal and polyclonal antibodies to determine differentiation antigens of leukocytes by the method of immunofluorescence microscopy from LLC Sorbent (Russia) in accordance with the manufacturer's instructions. To study the Ig class content of A, M, G serum, the method of simple radial immunodiffusion in the gel was used. The concentration of the CEC in the blood was determined according to Dijon. The results of the studies were processed by the method of variational and correlation statistics using the program "Statistica 10.0 for Windows", also methods of parametric and nonparametric statistics were used. It was found out that the immune response in patients with MI during the height of the disease was characterized by imbalance of the cell link (as evidenced by an increase in CD3+, CD4+, and a simultaneous increase in CD16+, CD25+), activation of the humoral unit (increase in CD20+, IgA, IgM, Ig G) immunity. In the period of reconvalescence in a larger number of patients with MI, the revealed disorders were continued to persist, not reaching the values of the control group. The obtained results testify significant changes in the structural characteristics of the cellular and humoral immune system and the multidirectionality of the immune response in acute and chronic course of the disease. The progressive nature of changes in immune parameters in both MI and HBEB indicates the formation of a secondary cellular immune imbalance, activation of the humoral link of immune defense, a change in the equilibrium of immunoregulatory mediators towards the Th2-link in the formation of chronic forms of EBV infection.

Keywords: Epstein-Barr virus, infectious mononucleosis, chronic forms of EBV infection, immune response

Full text: PDF (Ukr) 308K

References
  1. Cen О, Longnecker R. Latent Membrane Protein 2 (LMP2). Curr Top Microbiol Immunol. 2015; 391: 151–80. https://www.ncbi.nlm.nih.gov/pubmed/26428374. https://doi.org/10.1007/978-3-319-22834-1_5
  2. Drutskaya MS, Belousov PV, Nedospasov SA. Vrozhdennoye raspoznavaniye virusov. Molekulyarnaya biologiya. 2011; 45 (1): 7–19. [Russian].
  3. Griffin BD, Gram AM, Mulder A, Van Leeuwen D, Claas FH, Wang F, Ressing ME, Wiertz E. EBV BILF1 evolved to downregulate cell surface display of a wide range of HLA class I molecules through their cytoplasmic tail. J Immunology. 2013; 190: 1672–84. https://www.ncbi.nlm.nih.gov/pubmed/23315076. https://www.ncbi.nlm.nih.gov/pmc/articles/3565383. https://doi.org/10.4049/jimmunol.1102462
  4. Fathallah I, Parroche P, Gruffat H, Zannetti C, Johansson H, Yue J, Manet E, Tommasino M, Sylla BS, Hasan UA. EBV latent membrane protein 1 is a negative regulator of TLR9. J Immunology. 2010; 185: 6439–47. https://www.ncbi.nlm.nih.gov/pubmed/20980631. https://doi.org/10.4049/jimmunol.0903459
  5. Gaudreault E, Fiola S, Olivier M, Gosselin J. Epstein-Barr virus induces MCP-1 secretion by human monocytes via TLR2. J Virology. 2007; 81: 8016–24. https://www.ncbi.nlm.nih.gov/pubmed/17522215. https://www.ncbi.nlm.nih.gov/pmc/articles/1951286. https://doi.org/10.1128/JVI.00403-07
  6. Fish K, Chen J, Longnecker R. Epstein-Barr virus latent membrane protein 2A enhances MYC-driven cell cycle progression in a mouse model of B lymphoma. Blood. 2014; 123: 530–40. https://www.ncbi.nlm.nih.gov/pmc/articles/3901066. https://doi.org/10.1182/blood-2013-07-517649
  7. Fukuda M, Kawaguchi Y. Role of the immunoreceptor tyrosine-based activation motif of latent membrane protein 2A (LMP2A) in Epstein-Barr virus LMP2A-induced cell transformation. J Virology. 2014; 88: 5189–94. https://www.ncbi.nlm.nih.gov/pmc/articles/3993816. https://doi.org/10.1128/JVI.03714-13
  8. Gibson J, Gow N, Wong SY. Expression and Funktion of innate Pattent Recognition Receptors in T and B cells. Immun, Endoc&Metab Agents in Med Chem. 2010; 10: 11-20.
  9. Guerreiro M, Na IK, Letsch A, Haase D, Bauer S, Meisel C, Roemhild A, Reinke P, Volk HD, Scheibenbogen C. Human peripheral blood and bone marrow EBV-specific T-cell repertoire in latent infection reveals distinct memory T-cell subsets. Eur J Immune. 2010; 15: 1566-76. https://www.ncbi.nlm.nih.gov/pubmed/20232341. https://doi.org/10.1002/eji.200940000
  10. Isakov VA, Arkhipova EI, Isakov DV. Gerpesvirusnyye infektsii cheloveka: rukovodstvo dlya vrachey. SPb, 2006. 303 s. [Russian].
  11. Kawai T, Akira S. The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors. Nat Immunol. 2010; 11 (5): 373–84. https://www.ncbi.nlm.nih.gov/pubmed/20404851. https://doi.org/10.1038/ni.1863
  12. Krasnitskaya AS, Borovskaya NA. Immunologicheskiye aspekty khronicheskogo tonzillita, assotsiirovannogo s virus Epshteyna-Barr infektsiyey. Fundamentalnyye issledovaniya. 2012; 299–305. [Russian].
  13. Kudin AP. Eta «bezobidnaya» virus Epshtejna – Barr infekciya. Chast 1. Harakteristika vozbuditelya. Reakciya immunnoj sistemy na virus. Medicinskie novosti. 2006; 7: 25-32. [Russian].
  14. Thorley-Lawson DA, Hawkins JB, Tracy SI, Shapiro M. The pathogenesis of Epstein-Barr virus persistent infection. Curr Opin Virol. 2013. 3: 227–32. https://www.ncbi.nlm.nih.gov/pubmed/23683686. https://www.ncbi.nlm.nih.gov/pmc/articles/3789532. https://doi.org/10.1016/j.coviro.2013.04.005
  15. Tugizov S, Herrera R, Veluppillai P, Greenspan J, Greenspan D, Palefsky JM. Epstein-Barr Virus (EBV)-Infected Monocytes Facilitate Dissemination of EBV within the Oral Mucosal Epithelium. J Virol. 2007; 81 (11): 5484-96. https://www.ncbi.nlm.nih.gov/pmc/articles/1900306. https://doi.org/10.1128/JVI.00171-07
  16. Vozianova ZH, Hley AI. I. Infektsiyniy mononukleoz yak polietiolohichne zakhvoryuvannya. Suchasni infektsiyi. 2004; 2: 37-41. [Ukrainian].