Abstract

Objective: To study the effect of cytomegalovirus infection on histidine concentration in erythrocytes of peripheral blood in pregnant women at 27-28th week of gestation and virus penetration through the erythrocyte membrane and to demonstrate the morphofunctional alterations of the latter. The objective of this study is to demonstrate the mechanism of cytomegalovirus penetration through the erythrocyte membrane as well as to describe the process of its structure damage which leads to the accumulation in the peripheral blood of degenerative forms of erythrocytes that lose their ability to deformability. This creates the conditions for the formation of hemic anaemia in a pregnant woman. The research has been conducted on the basis of current data and our own studies. Materials and methods: 75 pregnant women at 27-28th weeks of gestation were examined, including 55 CMV-seropositive ones with CMV-infection exacerbation at 27th week of gestation. All the studies were carried out at the Federal State Budget Scientific Institution “Far Eastern Scientific Centre of Physiology and Pathology of Respiration” during one year time. Histidine activity in peripheral blood erythrocytes was found according to the method suggested by Lucenko Michael T and Andrievskaya Irina A.; fatty acid peroxides in erythrocyte membrane-by Winkler-Schultze method; erythrocyte membrane microviscosity was found by spectrofluorimetric method of lateral diffusion of pyrene. Erythrocyte deformability was also found in accordance with the method of Lucenko Michael T and Andrievskaya Irina A. The calculation of deformed erythrocytes was done using automated cytophotometric device “Mekos” (Russia). Erythrocyte membrane condensation was measured in pixels by means of cytophotometric camera “Pixera” (USA). Results: During the exacerbation of CMV infection at 27-28th weeks of gestation the amount of distal histidine was lower 2.13 times per one erythrocyte. The level of unsaturated fatty acids increased 2.9 times, of fatty acid peroxides in erythrocyte membranes increased 3.3 times, which resulted in 1.7 times increase in erythrocyte membrane microviscosity in the lipid bilayer and in 6.8 times increase in erythrocyte deformability. Conclusion: The exacerbation of chronic CMV infection at 27-28th weeks of gestation causes the virus intrusion into erythrocyte membrane damaging the distal histidine content, which promotes further penetration of proteins of viral envelope and tegument into the erythrocyte. That results in the disturbance of phospholipids bond with erythrocyte membrane proteins, increase in fatty acid peroxides in erythrocytes and decrease in the membrane microviscosity. This promotes the accumulation of deformable erythrocytes in peripheral blood thus causing the threat of anemia formation in pregnant woman at late gestation.

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