Corpus overview


Overview

MeSH Disease

Human Phenotype

There are no HP terms in the subcorpus


Transmission

Seroprevalence

There are no seroprevalence terms in the subcorpus

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    Prediction of non-canonical routes for SARS-CoV-2 infection MESHD in human placenta cells

    Authors: Flavia Bessi Constantino; Sarah Santiloni Cury; Celia Regina Nogueira; Robson Carvalho; Luis Justulin

    doi:10.1101/2020.06.12.148411 Date: 2020-06-12 Source: bioRxiv

    The SARS-CoV-2 is the causative agent of the COVID-19 pandemic. The data available about COVID-19 during pregnancy have demonstrated placental infection MESHD; however, the intrauterine transmission TRANS of SARS-CoV-2 is still debated. Intriguingly, while canonical SARS-CoV-2 cell entry mediators are expressed at low levels in placental cells, the receptors for viruses that cause congenital infections such as the cytomegalovirus MESHD and Zika virus are highly expressed in these cells. Here we analyzed the transcriptional profile (microarray and single-cell RNA-Seq) of proteins potentially interacting with coronaviruses to identify non-canonical mediators of SARS-CoV-2 infection MESHD and replication in the placenta. We show that, despite low levels of the canonical cell entry mediators ACE2 and TMPRSS2, villous trophoblast cells co-express high levels of the potential non-canonical cell-entry mediators DPP4 and CTSL. We also found changes in the expression of DAAM1 and PAICS genes during pregnancy, which are translated into proteins also predicted to interact with coronaviruses proteins. These results provide new insight into the interaction between SARS-CoV-2 and host proteins that may act as non-canonical routes for SARS-CoV-2 infection MESHD and replication in the placenta cells.

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MeSH Disease
Human Phenotype
Transmission
Seroprevalence


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