Abstract

There were investigated levels of pro-inflammatory and regulatory cytokines (IL-1b, IL-6 and IFN-g) in women of reproductive age in periods of exacerbation and remission of chronic infection caused by the herpes simplex virus in purpose to study the pathogenetic features of the course of HSV infection. It is shown that both the period of exacerbation, and the period of clinical remission of chronic herpes infection are characterized by increased production of IFN-g, IL-1b and IL-6. However, only the mean values of IL-1b were significantly different in periods of exacerbation and remission. Moreover, patients with chronic herpes infection revealed significant heterogeneity of individual values of measured cytokines (IL-1b, IL-6 and IFN-g), which does not depend on the period of clinical disease.

Highlights

  • The problem of infection caused by the herpes virus, is certainly relevant

  • Patients with chronic herpes infection revealed significant heterogeneity of individual values of measured cytokines (IL-1β, IL-6 and IFN-γ), which does not depend on the period of clinical disease

  • It should be noted that IL-1β has significantly higher means in both stages of a pathological process when compared with the standard values

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Summary

Introduction

The problem of infection caused by the herpes virus, is certainly relevant. The most common pathological conditions are caused by the herpes simplex virus types and 2 (HSV1, 2). This fact let us to speak about chronic HSV-infection caused by 1-st and 2-nd type viruses regardless of the localization of the process [5] [6]. Problem remains unclear why the infection does not occur in the complete elimination (eradication) of the virus Perhaps this “inadequate” response is determined by the biological properties of the virus: its low immunogenicity, the ability for mimicry and “escape” from the immune surveillance. These properties predispose to long-term persistence of the pathogen and the development of a chronic process [7]-[10]. Preservation of the virus in the host (latency) is the cause of recurrent exacerbations of the disease [11] [12]

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