SARS-CoV-2 seizes mitochondria function

SARS-CoV-2 is a positive-sense group β coronavirus. It is single-stranded with a genome of around 30 kbp. The genome of the virus contains ten open-reading frames (ORFs) that encode Spike, Membrane, Envelope, and the nucleocapsid proteins which are the four structural proteins, and six nonstructural proteins such as ORF1ab, ORF3, ORF6, ORF7, ORF8, and ORF10.
Research demonstrated that mitochondrial translation machinery plays an important phase in the viral protein translation. It was then widely understood that viruses effectively interact with mitochondrial receptors to inhibit mitochondrial antiviral signalling processes. This in turn this induces mitochondrial stress that facilitates the survival and replication of viruses. Mitochondrial vesicles are formed, that act as a replication niche for the virus as they regulate the production of ATP, cellular differentiation , apoptosis, and antiviral immune activation.
They concluded that Mitochondrial-targeting drugs have strong potential as antiviral therapeutic reagents as mitochondria-targets significantly repress rare codon-driven gene expression and viral replication.
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