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Viruses. 2021 Dec 19;13(12). doi: 10.3390/v13122545.

Intrauterine Fetal Demise After Uncomplicated COVID-19: What Can We Learn from the Case?.

Viruses

Pavel Babal, Lucia Krivosikova, Lucia Sarvaicova, Ivan Deckov, Tomas Szemes, Tatiana Sedlackova, Michal Palkovic, Anna Kalinakova, Pavol Janega

Affiliations

  1. Department of Pathology, Faculty of Medicine, Comenius University, 811 08 Bratislava, Slovakia.
  2. Department of Pathology, University Hospital, 917 75 Trnava, Slovakia.
  3. Department of Gynecology and Obstetrics, University Hospital, 917 75 Trnava, Slovakia.
  4. Laboratory of Genomics and Bioinformatics, Comenius University Science Park, 841 04 Bratislava, Slovakia.
  5. Health Care Surveillance Authority, 829 24 Bratislava, Slovakia.
  6. Public Health Authority of the Slovak Republic, 826 45 Bratislava, Slovakia.
  7. Centre of Experimental Medicine, Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, 813 71 Bratislava, Slovakia.

PMID: 34960815 PMCID: PMC8708385 DOI: 10.3390/v13122545

Abstract

BACKGROUND: SARS-CoV-2 infection in pregnant women can lead to placental damage and transplacental infection transfer, and intrauterine fetal demise is an unpredictable event.

CASE STUDY: A 32-year-old patient in her 38th week of pregnancy reported loss of fetal movements. She overcame mild COVID-19 with positive PCR test 22 days before. A histology of the placenta showed deposition of intervillous fibrinoid, lympho-histiocytic infiltration, scant neutrophils, clumping of villi, and extant infarctions. Immunohistochemistry identified focal SARS-CoV-2 nucleocapsid and spike protein in the syncytiotrophoblast and isolated in situ hybridization of the virus' RNA. Low ACE2 and TMPRSS2 contrasted with strong basigin/CD147 and PDL-1 positivity in the trophoblast. An autopsy of the fetus showed no morphological abnormalities except for lung interstitial infiltrate, with prevalent CD8-positive T-lymphocytes and B-lymphocytes. Immunohistochemistry and in situ hybridization proved the presence of countless dispersed SARS-CoV-2-infected epithelial and endothelial cells in the lung tissue. The potential virus-receptor protein ACE2, TMPRSS2, and CD147 expression was too low to be detected.

CONCLUSION: Over three weeks' persistence of trophoblast viral infection lead to extensive intervillous fibrinoid depositions and placental infarctions. High CD147 expression might serve as the dominant receptor for the virus, and PDL-1 could limit maternal immunity in placental tissue virus clearance. The presented case indicates that the SARS-CoV-2 infection-induced changes in the placenta lead to ischemia and consecutive demise of the fetus. The infection of the fetus was without significant impact on its death. This rare complication of pregnancy can appear independently to the severity of COVID-19's clinical course in the pregnant mother.

Keywords: SARS-CoV-2; fetal demise; persistent infection; syncytiotrophoblast; transplacental transmission

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