Abstract
The new type of pneumonia caused by the SARS-CoV-2 (Severe acute respiratory syndrome coronavirus 2) has been declared as a global public health concern by WHO. As of April 3, 2020, more than 1,000,000 human infections have been diagnosed around the world, which exhibited apparent person-to-person transmission characteristics of this virus. The capacity of vertical transmission in SARS-CoV-2 remains controversial recently. Angiotensin-converting enzyme 2 (ACE2) is now confirmed as the receptor of SARS-CoV-2 and plays essential roles in human infection and transmission. In present study, we collected the online available single-cell RNA sequencing (scRNA-seq) data to evaluate the cell specific expression of ACE2 in maternal-fetal interface as well as in multiple fetal organs. Our results revealed that ACE2 was highly expressed in maternal-fetal interface cells including stromal cells and perivascular cells of decidua, and cytotrophoblast and syncytiotrophoblast in placenta. Meanwhile, ACE2 was also expressed in specific cell types of human fetal heart, liver and lung, but not in kidney. And in a study containing series fetal and post-natal mouse lung, we observed ACE2 was dynamically changed over the time, and ACE2 was extremely high in neonatal mice at post-natal day 1~3. In summary, this study revealed that the SARS-CoV-2 receptor was widely spread in specific cell types of maternal-fetal interface and fetal organs. And thus, both the vertical transmission and the placenta dysfunction/abortion caused by SARS-CoV-2 need to be further carefully investigated in clinical practice.
Highlights
TMPRSS2 found a similar dynamic alteration (Fig 1C). These results suggest that Angiotensin-converting enzyme 2 (ACE2) and TMPRSS2 were co-expressed in villous cytotrophoblast (VCT), SCT and extravillous trophoblast (EVT) cells in maternal-fetal interface, and the expression level of ACE2/TMPRSS2 in maternalfetal interface may increase along with trimester of pregnancy
After the PND 1~3, ACE2 and TMPRSS2 recovered to relatively low level in lung and mainly expressed in epithelial cells, which is similar to that in adult human lung [22] (Fig 3B and 3C). These results suggest that the alternative expression of ACE2/TMPRSS2 in pulmonary cells before and after birth may contribute to the virus infection through vertical or respiratory transmission, and ACE2 and TMPRSS2 were highly co-expressed across different cell types of murine lung
The second, this study reported the distribution of ACE2 and TMPRSS2, but the existence of vertical transmission and placenta dysfunction caused by SARS-CoV-2 infection is just speculative, which needs to be further evaluated by clinical investigations
Summary
[1] The ongoing outbreak was first reported in Wuhan, China, in December 2019 and as of April 3, 2020 more than 1,000,000 human infections have been confirmed around the world. ACE2 is newly described as Renin-angiotensin system (RAS) component and modulates blood pressure.[6] The expression and distribution of ACE2 has been reported in heart, lungs and kidneys, which exhibits tissue-specific activity patterns.[7,8,9] Previous studies have shown the expression of ACE2 in the placenta.[10] the serine protease for virus Spike (S) protein priming, TMPRSS2, was identified to be indispensable for cell entry of SARS-CoV-2. The serine protease for virus Spike (S) protein priming, TMPRSS2, was identified to be indispensable for cell entry of SARS-CoV-2. [11]
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