ABSTRACT
Background. This study aimed to comprehensively evaluate the clinical characteristics of COVID-19 in perinatal period, and systematically assess the mother-to-child transmission potential of SARS-CoV-2Methods. We retrospectively analyzed the data of 23 pregnant patients in late pregnancy. Clinical specimens, including maternal and neonatal throat swabs, vaginal secretions, placenta tissues, and breast milk, were collected for the nucleic acid test of the virus. Pregnancy outcomes and neonatal results were also analyzed.Results. Overall, 10 patients (43.5%) had no symptoms and were found by routine chest CT. Complications appeared after COVID-19 onset included PROM (17.4%) and fetal distress (4.3%). Typical signs of viral pneumonia were recorded in chest CT of all patients. No patients developed severe pneumonia or died of COVID-19. All of 25 neonates were born alive. No severe asphyxia or neonatal death was observed. Although three neonates were tested transiently suspected positive for SARS-CoV-2 after being transferred to neonatology department, no newborns developed COVID-19. Out of various clinical specimens tested, only a rectal swab sample from one pregnant patient was tested positive for SARS-CoV-2, while all the other specimens including first sample of newborn throat swabs were negative. Pathological examination found no obvious chorioamnionitis or clear virus inclusion body in placenta, and ACE2 (angiotension-converting enzyme 2) was expressed at a moderate level.Conclusions. As in the general population of COVID-19, asymptomatic patients were present in pregnant women. There is no confirmatory evidence for mother-to-child transmission in COVID-19 patients with late pregnancy.
Subject(s)
Perinatal Death , Asphyxia , Pneumonia, Viral , Pneumonia , Chorioamnionitis , Breast Neoplasms , COVID-19ABSTRACT
We hereby reported the diagnosis, treatment process and perinatal outcome of a patient with novel coronavirus infection in perinatal period. The pregnant woman delivered a boy by cesarean section at 37+2 gestational weeks due to severe liver dysfunction. She subsequently had a high fever 2 days later, and novel coronavirus infection was confirmed by nucleic acid test in a throat swab. After a 12-day isolation and support treatment, her two consecutive throat swab results for novel coronavirus turned negative and she was discharged. The novel coronavirus was tested in the patient's blood, urine, breast milk as well as the neonatal throat swab, and the results were all negative. The neonate had an elevated myocardial enzyme, but was otherwise well and was discharged after 14-day isolation with normal myocardial enzyme.
ABSTRACT
There is pressing urgency to understand the pathogenesis of the severe acute respiratory syndrome coronavirus clade 2 (SARS-CoV-2) which causes the disease COVID-19. SARS-CoV2 spike (S)-protein binds ACE2, and in concert with host proteases, principally TMPRSS2, promotes cellular entry. The cell subsets targeted by SARS-CoV-2 in host tissues, and the factors that regulate ACE2 expression, remain unknown. Here, we leverage human, non-human primate, and mouse single-cell RNA-sequencing (scRNA-seq) datasets across health and disease to uncover putative targets of SARS-CoV-2 amongst tissue-resident cell subsets. We identify ACE2 and TMPRSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal goblet secretory cells. Strikingly, we discover that ACE2 is a human interferonstimulated gene (ISG) in vitro using airway epithelial cells, and extend our findings to in vivo viral infections. Our data suggest that SARS-CoV-2 could exploit species-specific interferon-driven upregulation of ACE2, a tissue-protective mediator during lung injury, to enhance infection.