Perinatal HIV infection and opportunistic infectious pathology: morphological features of the placenta

Opportunistic infections account for more than 90% of all deaths associated with immunosuppression resulting from exposure to the human immunodeficiency virus  (HIV). Fatal opportunistic infections  include Pneumocystis pneumonia, cryptococcosis, cytomegalovirus infection, and viral hepatitis B and/or C. HIV-infected pregnant women have a high incidence of cytomegalovirus infection, which increases the risk of transplacental transmission of HIV from mother to fetus. In addition, an important factor in perinatal transmission of HIV is a genital infection caused by herpes simplex virus type 2 detected during pregnancy in HIV-infected women. Also, at present, there is no doubt about the possibility of damage to placental cells by the SARS-CoV-2 virus and its transplacental transmission.

The aim of this study was to study the morphological features of the placenta in the presence of opportunistic infections caused by viruses of the herpes family (herpes simplex viruses types 1/2, cytomegalovirus, Epstein-Barr virus), as well as SARS-CoV2 in HIV-infected pregnant women.

Materials and methods. A study was conducted of 21 placentas with various pregnancy outcomes in HIV-infected women, including 12 placentas obtained as a result of term birth, 1 placenta from premature birth at 29 weeks, and 8 observations of failed miscarriages (non-developing pregnancy).

Results and discussion. Viral lesions were represented by the action of HIV with giant cell metamorphosis of trophoblast cells and placental macrophages, as well as infiltration by immunocompetent cells and fibrosis of the villous stroma. In addition, groups of immature villi were identified, the edematous stroma of which contained an increased number of large cells with light nuclei. In HIV-infected pregnant women with immunosuppression, the outcome of pregnancy in 8 cases was a miscarriage with a morphologically detected and immunohistochemically confirmed infection caused by herpes simplex virus types 1/2 (3 observations), cytomegalovirus (2 observations), and SARS-CoV-2 (3 observations), in 1 case the outcome of pregnancy was premature birth with morphologically identified and immunohistochemically confirmed infection caused by the Epstein-Barr virus.

Conclusion. The placentas of HIV-infected pregnant women are characterized by impaired villous maturation with stromal fibrosis, which is the morphological substrate of chronic placental insufficiency with varying degrees of compensation. If HIVinfected pregnant women have opportunistic infections caused by viruses of the herpes family (herpes simplex viruses types 1/2, cytomegalovirus, Epstein-Barr virus), as well as SARS-CoV-2, pronounced involutive-dystrophic changes are observed in the placentas — perivillous deposition fibrinoid, petrification, which increases the likelihood of an unfavorable pregnancy outcome in the form of miscarriage or premature birth.

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