Features of interferon system in patients with herpes zoster

Written by Knysh S.V., Malkov V.A., Prosekova E.V., Kovalchuk V.K.

  UDK: 616.834–002.152:612.017.1 | Pages: 34–37 | Full text PDF | Open PDF 


Objective. Study of mediators of immune system – is one of the main immunology direction. Interferons (IFN) are the most studied group of mediators. It includes three types of IFN – I type (α, β, ω) with marked antiviral activity, II type (γ) – whose main function is immune regulation. And III type (λ1, λ2, λ3, and λ4) with antitumor and antiviral activity. The aim of work: to study condition of IFN system by evaluating the serum level of IFN’s in patients with herpes zoster.
Methods. 50 patients with herpes zoster were examined. Serum was taken in first 72 hours after disease manifestation. The level of IFN‑β, IFN‑γ, IFN‑λ1, IFN‑λ3, IFN‑λ1/3 was determined by using specific reagents R&D Diagnostics Inc. (USA). The data were presented as a median and two quartiles (Me, Q25, Q75). The interrelation of indicators was estimated by the Spearman correlation coefficient.
Results. The serum level of IFN‑β, IFN‑λ1, IFN‑λ3, IFN‑λ1/3 were significantly lower in patients with herpes zoster in comparison with the control group. Also, the weak positive correlation between IFN‑β and IFN‑λ1/3, IFN‑β and IFN‑γ; and medium positive correlation between IFN‑γ and IFN‑λ1/3 were established.
Conclusions. The interferons deficiency was identified. Presumably the correlation between IFN‑γ and IFN‑λ1/3 is due to common type of producer cell – plasmacytoid dendritic cells. In addition, the direct positive effect of IFN‑λ on interleukin-12 (IL-12) and on NK-cells through IL-12 cause positive effect of IFN‑λ to IFN‑γ. Disbalance in interferons ratio – one of the potent factors of varicella zoster virus reactivation. In addition, the high serum level of IFN‑γ is a factor of mild course of disease.

Links to authors:

S.V. Knysh, V.A. Malkov, E.V. Prosekova, V.K. Kovalchuk
Pacific State Medical University (2 Ostryakova Ave. Vladivostok 690002 Russian Federation)

1. Knysh S.V., Markelova E.V., T.A. Nevezhkina [et al.]. Serum IFN-lambda and IFN-gamma of herpes zoster patients // Russian Journal of Immunology. 2017. Vol. 11, No. 4. P. 712–714.
2. Simbirtsev A.S. Cytokines in the pathogenesis and treatment of human diseases. Saint Petersburg: Foliant, 2018. 512 p.
3. Sklyar L.F., Markelova E.V., Nagornaya A.V., Sotnichenko S.A. Clinical features and the natural immunity state of the HIVinfected patients having herpes meningoencephalitis // Pacific Medical Journal. 2014. No. 1. P. 82–85.
4. Ank N., West H., Bartholdy C. [et al.]. Lambda interferon (IFN‑λ), a type III IFN, is induced by viruses and IFNs and displays potent antiviral activity against select virus infections in vivo // Journal of Virology. 2006. Vol. 80, No. 9. P. 4501–4509.
5. Baird N.L., Bowlin J.L., Hotz T.J. [et al.]. Interferon gamma prolongs survival of Varicella-Zoster virus infected human neurons in vitro // Journal of Virology. 2015. Vol. 89, No. 14. P. 7425–7427.
6. Groen R.A., Boltjes A., Hou J. [et al.]. IFN‑λ-mediated IL-12 production in macrophages induces IFN‑γ production in human NK cells // Eur. J. Immunol. 2015. No. 45. P. 250–259.
7. Kim C.K., Choi Y.M., Bae E. [et al.]. Reduced NK cell IFN‑γ secretion and psychological stress are independently associated with herpes zoster. // PLoS ONE. Vol. 13, No 2. P. e0193299.
8. Ku C.C., Chang Y.H., Chien Y., Lee T.L. Type I interferon inhibits varicella-zoster virus replication by interfering with the dynamic interaction between mediator and IE62 within replication compartments // Cell Biosci. 2016. Vol. 6 doi: 10.1186/s13578-016-0086-6.
9. Li J., Ye L., Wang X. [et al.]. Induction of IFN-lambda contributes to TLR3-mediated HSV-1 inhibition in astrocytes // J. Neurosci. Res. 2012. Vol. 90, No. 2. P. 399–406.
10. Misumi I., Whitmire J.K. FN-lambda exerts opposing effects on T cell responses depending on the chronicity of the virus infection // J. Immunol. 2014. Vol. 192, No. 8. P. 3596–3606.
11. Ng C.T., Sullivan B.M, Teijaro J.R. [et al.]. Blockade of interferon beta, but not interferon alpha, signaling controls persistent viral infection // Cell Host Microbe. 2015. Vol. 17, No 5. P. 653–661.
12. Petersen T., Moller-Larsen A., Ellermann-Eriksen S. [et al.]. Effects of interferon-beta therapy on elements in the antiviral immune response towards the human herpesviruses EBV, HSV, and VZV, and to the human endogenous retroviruses HERV-H and HERV-W in multiple sclerosis // Journal of Neuroimmunology. 2012. No. 249. P. 105–108.
13. Read S.A., O’Connor K.S., Suppiah V. [et al.]. Zinc is a potent and specific inhibitor of IFN‑λ3 signalling // Nature communications. 2017. Vol 8. doi: 10.1038/ncomms15245 (2017).
14. Sen N., Arvin, A.M. Dissecting the molecular mechanisms of the tropism of Varicella-Zoster virus for human T cells // Journal of Virology. 2016. Vol. 90, No. 7. P. 3284–3287.
15. Yin Z., Dai J., Deng J. [et al.]. Type III IFNs are produced by and stimulate human plasmacytoid dendritic cells // J. Immunol. 2012. Vol. 189, No. 6. P. 2735–2745.


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