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Deciphering the co-adaptation of codon usage between respiratory coronaviruses and their human host uncovers candidate therapeutics for COVID-19.

ABSTRACT: Coronavirus disease 2019 (COVID-19) has caused thousands of deaths worldwide and has become an urgent public health concern. The extraordinary interhuman transmission of this disease has urged scientists to examine the various facets of its pathogenic agent, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Herein, based on publicly available genomic data, we analyzed the codon usage co-adaptation profiles of SARS-CoV-2 and other respiratory coronaviruses (CoVs) with their human host, identified CoV-responsive human genes and their functional roles on the basis of both the relative synonymous codon usage (RSCU)-based correlation of viral genes with human genes and differential gene expression analysis, and predicted potential drugs for COVID-19 treatment based on these genes. The relatively high codon adaptation index (CAI) values (>0.70) signposted the gene expressivity efficiency of CoVs in human. The ENc-GC3 plot indicated that SARS-CoV-2 genome was under strict selection pressure while SARS-CoV and MERS-CoV were under selection and mutational pressures. The RSCU-based correlation analysis indicated that the viral genomes shared similar codons with a panoply of human genes. The merging of RSCU-based correlation data and SARS-CoV-2-responsive differentially expressed genes allowed the identification of human genes potentially affected by SARS-CoV-2 infection. Functional enrichment analysis indicated that these genes were enriched in biological processes and pathways related to host response to viral infection and immune response. Using the drug-gene interaction database, we screened a list of drugs that could target these genes as potential COVID-19 therapeutics. Our findings not only will contribute in vaccine development but also provide a useful set of drugs that could guide practitioners in strategical monitoring of COVID-19. We recommend practitioners to scrupulously screen this list of predicted drugs in order to authenticate those qualified for treating COVID-19 symptoms.

SUBMITTER: Nambou K

PROVIDER: S-EPMC7374176 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

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Deciphering the co-adaptation of codon usage between respiratory coronaviruses and their human host uncovers candidate therapeutics for COVID-19.

Nambou Komi K Anakpa Manawa M

Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases 20200722

Coronavirus disease 2019 (COVID-19) has caused thousands of deaths worldwide and has become an urgent public health concern. The extraordinary interhuman transmission of this disease has urged scientists to examine the various facets of its pathogenic agent, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Herein, based on publicly available genomic data, we analyzed the codon usage co-adaptation profiles of SARS-CoV-2 and other respiratory coronaviruses (CoVs) with their human ...[more]

PMID: 32707288

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Project description:BACKGROUND: The ISA virus (ISAV) is an Orthomyxovirus whose genome encodes for at least 10 proteins. Low protein identity and lack of genetic tools have hampered the study of the molecular mechanism behind its virulence. It has been shown that viral codon usage controls several processes such as translational efficiency, folding, tuning of protein expression, antigenicity and virulence. Despite this, the possible role that adaptation to host codon usage plays in virulence and viral evolution has not been studied in ISAV. METHODS: Intergenomic adaptation between viral and host genomes was calculated using the codon adaptation index score with EMBOSS software and the Kazusa database. Classification of host genes according to GeneOnthology was performed using Blast2go. A non parametric test was applied to determine the presence of significant correlations among CAI, mortality and time. RESULTS: Using the codon adaptation index (CAI) score, we found that the encoding genes for nucleoprotein, matrix protein M1 and antagonist of Interferon I signaling (NS1) are the ISAV genes that are more adapted to host codon usage, in agreement with their requirement for production of viral particles and inactivation of antiviral responses. Comparison to host genes showed that ISAV shares CAI values with less than 0.45% of Salmo salar genes. GeneOntology classification of host genes showed that ISAV genes share CAI values with genes from less than 3% of the host biological process, far from the 14% shown by Influenza A viruses and closer to the 5% shown by Influenza B and C. As well, we identified a positive correlation (p<0.05) between CAI values of a virus and the duration of the outbreak disease in given salmon farms, as well as a weak relationship between codon adaptation values of PB1 and the mortality rates of a set of ISA viruses. CONCLUSIONS: Our analysis shows that ISAV is the least adapted viral Salmo salar pathogen and Orthomyxovirus family member less adapted to host codon usage, avoiding the general behavior of host genes. This is probably due to its recent emergence among farmed Salmon populations.

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Deciphering the co-adaptation of codon usage between respiratory coronaviruses and their human host uncovers candidate therapeutics for COVID-19.

Publications

Deciphering the co-adaptation of codon usage between respiratory coronaviruses and their human host uncovers candidate therapeutics for COVID-19.

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