Herpesvirus infection is associated with an increase of LPO and of the membrane lipid and lipid-protein layers microviscosity in erythrocyte membranes of pregnant patients. This results in modification of the erythrocyte stromal protein composition. Erythrocyte deformability increases sharply under these conditions, this leading to disorders in tissue metabolism in the organs of pregnant patients.
Exacerbation of herpesvirus infection during pregnancy is associated with damage to syncytiotrophoblast inflicted by herpesvirus either directly or via TNF-α (due to contact of NK lymphocytes with villus surface). A sharp decrease in the content of heat shock protein with a molecular weight of 70 Da and activation of caspase-3 were noted in placenta homogenate. This leads to disturbances in syncytiotrophoblast cytosol structure and increase in the relative content of apoptotic nuclei.
Enzymatic activity of the peripheral blood erythrocytes was studied in pregnant women after exacerbation of herpesvirus infection during the third trimester. Herpetic infection suppressed ATP synthesis and reduced the activities of glutathione reductase and glutathione peroxidase in erythrocytes. These shifts were paralleled by lesser intensity of SOD reaction, normally suppressing LPO processes in erythrocyte membranes.
Serotonin metabolism in the blood and placental homogenate was studied in pregnancy aggravated by exacerbation of herpesvirus infection. Blood serotonin content in pregnant patients increased with increasing herpesvirus antibody titers and reduction of monoamine oxidase activity. Urinary excretion of 5-hydroxyindoleacetic acid (5-HIAA) decreased. The decrease of monoamine oxidase activity in placental homogenate led to an increase of serotonin level, which was paralleled by destruction of mitochondria in the syncytiotrophoblast, suppression of BCL-2 protein activity, and increase of caspase-3 level.
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