HIV infection in pregnant women often becomes the cause of chronic inflammation in all organs and systems, including the placenta and significantly increases the level of vertical transmission of the virus. In the pathogenesis of inflammatory processes, especially in the presence of HIV, cytokines play an important role. Thus, the study of the morphofunctional state of the afterbirth in HIV infection facilitates identification of causes and mechanisms of placental insufficiency, as well as successful pathogenetic therapy and prophylaxis. The purpose of the research is evaluation of interleukin expression (IL-2, IL-4 and IL-1) in the structures of the placental barrier in HIV-infected women. The course of pregnancy, childbirth and perinatal period were studied and analyzed, as well as morphological immunohistochemical tests of afterbirths were made.
The material was presented by 55 cases of pregnancy, of which 10 cases were with the physiological course (10 afterbirths). The rest were divided into three groups, depending on the route of HIV infection and the use of antiretroviral therapy.
On microscopic examination abnormal placental immaturity, significant hemodynamic abnormalities and inflammatory processes in the afterbirths were revealed.
Investigation of the relative density of cytokine-producing cells showed that all the major groups of observations showed a tendency for a decrease in this indicator among proinflammatory IL-2 and IL-1 cell-producers, as well as an increase in the relative density of anti-inflammatory IL-4 cell-producers, especially in the group without injecting the infection — (3.30±0.29)%. Thus, the identified structural changes in the placenta and immunohistochemical changes in the afterbirths indicate the development of placental insufficiency in all cases and significant immunnopathological changes, that negatively affect the condition of the newborn child.