Fetoplacental transmission and placental response to SARS-CoV-2: Evidence from the literature.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a dreadful novel coronavirus with global health concerns among pregnant women. To date, the vertical transmission of SARS-CoV-2 during pregnancy remains controversial. We briefly report recent findings of placental response to SARS-CoV-2 infection and updates on vertical transmission. We systematically searched PubMed and Google Scholar databases according to PRISMA guidelines for studies reporting the effects of SARS-CoV-2 infection on the placenta and possibility of vertical transmission. We identified 45 studies reporting 1,280 human placentas that were analyzed by molecular pathology methods and 11,112 placenta-derived cells from a publicly available database that was analyzed using bioinformatics tools. The main finding of this study is that the SARS-CoV-2 canonical entry receptors (ACE2 and TMPRSS2) are abundantly expressed on the placenta during the first trimester, and this expression diminishes across gestational age. Out of 45 eligible studies identified, 24 (53.34%) showed no evidence of vertical transmission, 15 (33.33%) supported the hypothesis of very rare, low possibility of vertical transmission and 6 (13.33%) were indecisive and had no comment on vertical transmission. Furthermore, 433 placentas from 12 studies were also identified for placental pathology investigation. There was evidence of at least one form of maternal vascular malperfusion (MVM), 57/433 (13.1%), fetal vascular malperfusion (FVM), 81/433 (18.7%) and placental inflammation with excessive infiltration of CD3+ CD8+ lymphocytes, CD68+ macrophages and CD20+ lymphocytes in most of the eligible studies. Decidual vasculopathy (3.2%), infarction (3.2%), chronic histiocytic intervillositis (6.0%), thrombi vasculopathy (5.1%) were also observed in most of the MVM and FVM reported cases. The results indicated that SARS-CoV-2 induces placenta inflammation, and placenta susceptibility to SARS-CoV-2 decreases across the pregnancy window. Thus, SARS-CoV-2 infection in early pregnancy may adversely affect the developing fetus.

Lung microbiota dysbiosis and the implications of SARS-CoV-2 infection in pregnancy.

There are a great number of beneficial commensal microorganisms constitutively colonizing the mucosal lining of the lungs. Alterations in the microbiota profile have been associated with several respiratory diseases such as pneumonia and allergies. Lung microbiota dysbiosis might play an important role in the pathogenic mechanisms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as well as elicit other opportunistic infections associated with coronavirus disease 2019 (COVID-19). With its increasing prevalence and morbidity, SARS-CoV-2 infection in pregnant mothers is inevitable. Recent evidence shows that angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) act as an entry receptor and viral spike priming protein, respectively, for SARS-CoV-2 infection. These receptor proteins are highly expressed in the maternal-fetal interface, including the placental trophoblast, suggesting the possibility of maternal-fetal transmission. In this review, we discuss the role of lung microbiota dysbiosis in respiratory diseases, with an emphasis on COVID-19 and the possible implications of SARS-CoV-2 infection on pregnancy outcome and neonatal health.