Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


SARS-CoV-2 Proteins
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    A novel viral protein translation mechanism reveals mitochondria as a target for antiviral drug development

    Authors: Zhenguo Cheng; Danhua Zhang; Jingfei Chen; Yifan Wu; Lingling Si; Zhe Zhang; Na Zhang; Zhongxian Zhang; Hong Liu; Lirong Zhang; Lijie Song; Louisa S Chard Dunmall; Jianzeng Dong; Nicholas R Lemoine; Yaohe Wang; Daniel Cordero; Daniela Solano; Gina Durán; Eduardo Segura; Maykel Cerdas; Deibid Umaña; Edwin Moscoso; Ricardo Estrada; Jairo Gutiérrez; Marcos Méndez; Ana Cecilia Castillo; Laura Sánchez; José María Gutiérrez; Cecilia Díaz; Alberto Alape

    doi:10.1101/2020.10.19.344713 Date: 2020-10-19 Source: bioRxiv

    The ongoing Severe Acute Respiratory Syndrome coronavirus 2 MESHD (SARS-CoV-2) pandemic has acutely highlighted the need to identify new treatment strategies for viral infections MESHD. Here we present a pivotal molecular mechanism of viral protein translation that relies on the mitochondrial translation machinery. We found that rare codons such as Leu-TTA are highly enriched in many viruses, including SARS-CoV-2, and these codons are essential for the regulation of viral protein expression. SARS-CoV-2 controls the translation of its spike gene by hijacking host mitochondria through 5' leader and 3'UTR sequences that contain mitochondrial localization signals and activate the EGR1 HGNC pathway. Mitochondrial-targeted drugs such as lonidamine and polydatin significantly repress rare codon-driven gene expression and viral replication. This study identifies an unreported viral protein translation mechanism and opens up a novel avenue for developing antiviral drugs.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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