Background and aims Human herpesvirus 6 (HHV-6) is one of the causes of perinatal mortality and severe clinical conditions in newborn babies.
Aim To assess indices of the adaptive immune response in newborn babies with HHV-6.
Methods 58 newborn babies with a severe form of HHV-6 infection and 53 relatively healthy newborn babies were examined. The expression of membrane markers of CD3+, CD4+, CD8+, CD16+ and CD19+ immunocompetent cells in the peripheral blood was determined using Beckman Co.ulter Epics XL II flow laser cytometer (USA), (No. 20123). The lymphocyte typing was realised by means of homogeneous antibodies to the clusters of differentiation CD3+, CD4+, CD8+, CD16+ and CD19+ of IMMUNOTECH Company (France).
Results In the newborn babies with a severe form of HHV-6 infection as compared to the control group there was reduction of the total amount of CD3+ T-lymphocytes [55.25 (48.67–60.17)% and 65.2 (60.2–66.3)% correspondingly] (p < 0.05) and increase of CD8+ cytotoxic lymphocytes [28.2 (25.4–33.2)% and 20.3 (19.9–22.1)%] correspondingly (p < 0.05). In case of HHV-6 infection we also registered significant reduction of lymphocytes possessing helper-inductor properties (CD4) as compared to the control group [35.3 (33.2–38.4)% and 44.3 (41.6–46.4)% correspondingly] (p < 0.05). The comparison of average values of natural killer cells (CD16+) revealed significant decrease of their quantity as against the control group [2.3 (1.3–2.6)% and 4.2 (3.5–4.75)% correspondingly] (p < 0.05). The content of B-lymphocytes in the babies with a severe form of HHV-6 infection (CD19+) was significantly higher than that of the control group [12.4 (10.3–14.9)% and 2.7 (2.3–3.5)% correspondingly] (p < 0.05).
Conclusions The reaction of the immune system to HHV-6 infection in newborn babies is characterised by redistribution of the main T-lymphocyte subsets against the background of the reduced relative level of CD3+ and it declares itself by the reduction of the relative number of CD4+ and CD16+ that indicates the formation of secondary immunodeficiency of the cell type. It is also characterised by the increase of the activity level of lymphocytes with CD8 phenotype possessing helper-inductor properties, which is a control factor in the period of active viremia.
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