Garcia-Flores Valeria, Romero Roberto, Xu Yi, Theis Kevin, Arenas-Hernandez Marcia, Miller Derek, Peyvandipour Azam, Galaz Jose, Levenson Dustyn, Bhatti Gaurav, Gershater Meyer, Pusod Errile, Kracht David, Florova Violetta, Leng Yaozhu, Tao Li, Faucett Megan, Para Robert, Hsu Chaur-Dong, Zhang Gary, Tarca Adi L, Pique-Regi Roger, Gomez-Lopez Nardhy
Perinatology Research Branch, Division of Obstetrics and Maternal-Fetal Medicine, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, U.S. Department of Health and Human Services (NICHD/NIH/DHHS); Bethesda, Maryland, 20892 and Detroit, Michigan, 48201, USA.
Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, Michigan, 48201, USA.
Res Sq. 2021 Mar 31:rs.3.rs-362886. doi: 10.21203/rs.3.rs-362886/v1.
Pregnant women are a high-risk population for severe/critical COVID-19 and mortality. However, the maternal-fetal immune responses initiated by SARS-CoV-2 infection, and whether this virus is detectable in the placenta, are still under investigation. Herein, we report that SARS-CoV-2 infection during pregnancy primarily induced specific maternal inflammatory responses in the circulation and at the maternal-fetal interface, the latter being governed by T cells and macrophages. SARS-CoV-2 infection during pregnancy was also associated with a cytokine response in the fetal circulation (i.e. umbilical cord blood) without compromising the cellular immune repertoire. Moreover, SARS-CoV-2 infection neither altered fetal cellular immune responses in the placenta nor induced elevated cord blood levels of IgM. Importantly, SARS-CoV-2 was not detected in the placental tissues, nor was the sterility of the placenta compromised by maternal viral infection. This study provides insight into the maternal-fetal immune responses triggered by SARS-CoV-2 and further emphasizes the rarity of placental infection.
孕妇是感染新冠病毒后出现重症/危重症及死亡的高危人群。然而,SARS-CoV-2感染引发的母胎免疫反应,以及该病毒是否可在胎盘内检测到,仍在研究中。在此,我们报告孕期SARS-CoV-2感染主要在循环系统及母胎界面诱导了特异性母体炎症反应,后者由T细胞和巨噬细胞调控。孕期SARS-CoV-2感染还与胎儿循环系统(即脐带血)中的细胞因子反应有关,且未影响细胞免疫谱。此外,SARS-CoV-2感染既未改变胎盘内的胎儿细胞免疫反应,也未导致脐带血IgM水平升高。重要的是,在胎盘组织中未检测到SARS-CoV-2,且母体病毒感染未损害胎盘的无菌状态。本研究深入探讨了SARS-CoV-2引发的母胎免疫反应,并进一步强调了胎盘感染的罕见性。