The role of Herpesviridae infection in the progression of comorbid somatic pathology
Keywords:Herpesviridae infection, Herpes simplex virus, cytomegalovirus, chronic obstructive pulmonary disease, metabolic syndrome
Background. The objective was to study the peculiarities of cellular and humoral immunity in patients with chronic obstructive pulmonary disease (COPD) group B and C, GOLD 2–3, who have signs of metabolic syndrome (MS) and Herpesviridae infection. Materials and methods. Forty-two patients with B and C groups of COPD, GOLD 2–3, associated with MS were examined. Eighteen individuals had COPD combined with MS, and Herpesviridae infection. The average age of patients was 51.3 ± 4.2 years. The comparison group included 24 people with COPD and MS without signs of Herpesviridae infection. All patients underwent determination of herpes simplex virus (HSV) type 1 and cytomegalovirus (CMV) antigens in the blood and saliva, titer of specific immunoglobulin (Ig) G and IgM antibodies to HSV type 1 and CMV, a comprehensive immunological examination with a study of cellular and humoral immunity indexes, cytokine status. Results. The study of the activity of herpes viruses in the blood of patients of the main group did not reveal active replication of HSV type 1 and CMV; in the saliva of 15 individuals (83.3 %), an active replication of HSV type 1 was detected, and in 12 people (66.7%) — of CMV. All patients in the main group had a severe course of Herpesviridae infection with an exacerbation rate of more than 6 times a year. The immunological status of patients of the main group showed immunodeficiency mainly of T-cell immune system and NK-cells, a significant increase in the relative number of T- and B-lymphocytes with early and late markers of activation on the background of autoimmune manifestations and inflammatory changes in peripheral blood. Conclusions. The presence of chronic persistent infection of HSV type 1 and CMV causes a severe course of COPD associated with MS, induces the development of infectious exacerbations of COPD and more significant manifestations of systemic inflammation in atherosclerosis as a morphological substrate of MS.
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