5/28/2023 0 Comments 3hub virus![]() SARS-CoV-2, however, can hijack IFITM1, IFITM2, and IFITM3 to enhance the infection of the viruses thus, IFITMs serve as factors helping the entry of SARS-CoV-2 into cells. Additionally, in response to virus entry, cells usually express interferon-induced transmembrane proteins (IFITMs) that block the fusion capacity of many enveloped RNA viruses. The SARS-CoV-2 S protein has been found to be cleaved by several host cell proteases, including CTSL, FURIN, TMPRSS4, and TMPRSS11A. The results have shown that MERS receptor DPP4, SARS-CoV receptors CLEC4G/M, and HCoV-229E receptor CD13 cannot be SARS-CoV-2 receptors because of their inability to bind with SARS-CoV-2. Additionally, recent studies have tested whether other coronavirus (SARS-CoV, MERS-CoV, and HCoV) receptors work as SARS-CoV-2 receptors. The cell-surface receptors neuropilin-1 NRP1 and CD209 also facilitate the entry of SARS-CoV-2 to specific cells. However, ACE2 is not the only functional receptor for SARS-CoV-2. Therefore, many studies have revealed a subset of tissues and cell types that are potentially susceptible to SARS-CoV-2 using single-cell RNA-seq (scRNA-seq) and immunocytochemistry for profiling the co-expression of ACE2 and TMPRSS2 across healthy human tissues. The co-expression of ACE2 and TMPRSS2 is widely used as a marker for identifying cells that have the potential to be infected by SARS-CoV-2. SARS-CoV-2 infection in cells (SARS-CoV-2 cellular tropism) is caused by the binding of the viral spike (S) proteins to cellular receptors (e.g., angiotensin-converting enzyme 2 ACE2) and S protein priming by host cell proteases (e.g., transmembrane protease serine protease 2 TMPRSS2). ![]() Altogether, our work provides valuable cell-type-specific TRN models for understanding the transcriptional regulation and gene expression of SARS-CoV-2 tropism factors. In addition, we identified the TFs with high centralities from each cell type and proposed currently available drugs that target these TFs as potential candidates for the treatment of SARS-CoV-2 infection. Through differential network analysis, we found that the altered regulatory role of TFs in the same cell types of healthy and SARS-CoV-2-infected networks may be partially responsible for differential tropism factor expression. We constructed transcriptional regulatory networks (TRNs) controlling SARS-CoV-2 tropism factors for healthy donors and COVID-19 patients using lung single-cell RNA-sequencing (scRNA-seq) data. In this study, we used computational approaches to identify transcription factors (TFs) regulating SARS-CoV-2 tropism for different types of lung cells. Though previous studies have suggested that SARS-CoV-2 cellular tropism depends on the host-cell-expressed proteins, whether transcriptional regulation controls SARS-CoV-2 tropism factors in human lung cells remains unclear. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the virus that caused the coronavirus disease 2019 (COVID-19) pandemic. ![]()
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