Abstract
The novel coronavirus (2019-nCoV) has recently emerged, causing COVID-19 outbreaks and significant societal/global disruption. Importantly, COVID-19 infection resembles SARS-like complications. However, the lack of knowledge about the underlying genetic mechanisms of COVID-19 warrants the development of prospective control measures. In this study, we employed whole-genome alignment and digital DNA–DNA hybridization analyses to assess genomic linkage between 2019-nCoV and other coronaviruses. To understand the pathogenetic behavior of 2019-nCoV, we compared gene expression datasets of viral infections closest to 2019-nCoV with four COVID-19 clinical presentations followed by functional enrichment of shared dysregulated genes. Potential chemical antagonists were also identified using protein–chemical interaction analysis. Based on phylogram analysis, the 2019-nCoV was found genetically closest to SARS-CoVs. In addition, we identified 562 upregulated and 738 downregulated genes (adj. P ≤ 0.05) with SARS-CoV infection. Among the dysregulated genes, SARS-CoV shared ≤19 upregulated and ≤22 downregulated genes with each of different COVID-19 complications. Notably, upregulation of BCL6 and PFKFB3 genes was common to SARS-CoV, pneumonia and severe acute respiratory syndrome, while they shared CRIP2, NSG1 and TNFRSF21 genes in downregulation. Besides, 14 genes were common to different SARS-CoV comorbidities that might influence COVID-19 disease. We also observed similarities in pathways that can lead to COVID-19 and SARS-CoV diseases. Finally, protein–chemical interactions suggest cyclosporine, resveratrol and quercetin as promising drug candidates against COVID-19 as well as other SARS-like viral infections. The pathogenetic analyses, along with identified biomarkers, signaling pathways and chemical antagonists, could prove useful for novel drug development in the fight against the current global 2019-nCoV pandemic.
Highlights
During the past century, several human coronaviruses have emerged, causing severe respiratory illness and global outbreaks in humans [1]
Upregulation of BCL6 and PFKFB3 genes was common to SARS-CoV, pneumonia and severe acute respiratory syndrome, while they shared CRIP2, NSG1 and TNFRSF21 genes in downregulation
Due to the genetic closeness and unavailability of COVID-19-related datasets, we used microarray datasets related to SARS-CoV infection and four COVID-19 complications, i.e. pneumonia (PNA), severe acute respiratory syndrome (SARS), shortness of breath (SHOB) and diarrhea (DRA)
Summary
Several human coronaviruses have emerged, causing severe respiratory illness and global outbreaks in humans [1]. Two other coronaviruses, namely, severe acute the respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), have plagued the general public and caused global outbreaks in 2003 and 2012, respectively [1, 2]. In the late December 2019, a novel coronavirus (2019-nCoV), which may have evolved through host-induced natural selection [4], was first identified in patients with viral pneumonia in Wuhan City, China [1, 2]. As of 30 April 2020, there has been a total of 3 200 414 confirmed 2019nCoV cases and a death toll of 226 893 across 210 countries and territories (https://worldometers.info/coronavirus/). The disease outbreak is named as coronavirus disease 19 (COVID-19) [7]
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