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Abstract
Coronavirus disease 2019 (COVID-19) is an emerging infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and has posed a serious threat to global health. Here, we systematically characterized the transcription levels of the SARS-CoV-2 genes and identified the responsive human genes associated with virus infection. We inferred the possible biological functions of each viral gene and depicted the functional landscape based on guilt-by-association and functional enrichment analyses. Subsequently, the transcription factor regulatory network, protein–protein interaction network, and non-coding RNA regulatory network were constructed to discover more potential antiviral targets. In addition, several potential drugs for COVID-19 treatment and prevention were recognized, including known cell proliferation-related, immune-related, and antiviral drugs, in which proteasome inhibitors (bortezomib, carfilzomib, and ixazomib citrate) may play an important role in the treatment of COVID-19. These results provided novel insights into the understanding of SARS-CoV-2 functional genomics and host-targeting antiviral strategies for SARS-CoV-2 infection.
Highlights
Coronavirus disease 2019 (COVID-19) is an emerging infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and has posed a serious threat to global health
A set of subgenomic mRNAs are produced during the SARS-CoV-2 replication, including the structural protein mRNAs (S, M, E, and N) and other small accessory protein mRNAs
To better understand the host transcriptional response to SARS-CoV-2, we interrogated the viral gene-related human genes based on the linear regression model, which was constructed between the transcription levels of differentially expressed human gene i (H) and viral gene j (V) and corrected for the effect of cell types and MOI as co-variables, i.e., Hi ∼ α ∗ Vj + β + ε (Additional file 1)
Summary
Coronavirus disease 2019 (COVID-19) is an emerging infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), and has posed a serious threat to global health. Compared with other viral genes, the nucleocapsid (N) gene expression level was the highest and ORF7b was the lowest in all SARSCoV-2-infected cells (Fig. 1A). To better understand the host transcriptional response to SARS-CoV-2, we interrogated the viral gene-related human genes based on the linear regression model, which was constructed between the transcription levels of differentially expressed human gene i (H) and viral gene j (V) and corrected for the effect of cell types and MOI as co-variables, i.e., Hi ∼ α ∗ Vj + β + ε (Additional file 1).
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