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These recent developments, combined with our observation that complex II inhibition via the succinate dehydrogenase is a druggable and highly potent target for broad-spectrum antiviral inhibition, raise the possibility for the rapid establishment of novel broadly acting antiviral drugs

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General mitochondrial trifunctional protein (TFP) deficiency as a result of either alpha- or beta-subunit mutations exhibits similar phenotypes because mutations in either subunit alter TFP complex expression and subunit turnover

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