Key result
Infection with L-deficient cardiovirus mutants resulted in early caspase activation, cytochrome c efflux, and apoptosis, whereas wild-type virus elicited a strong antiapoptotic state.
Population
HeLa cells infected with encephalomyocarditis virus (a cardiovirus)
Comparison
Wild-type encephalomyocarditis virus vs L-deficient encephalomyocarditis virus
Design
Preclinical
Authors
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Animal data position L protein as apoptosis suppressor; leaves open relevance to human cardiovirus disease.
The cardiovirus leader (L) protein acts as a 'security protein' that suppresses host cell apoptosis during infection.
Romanova et al. (2009) studied Cardiovirus infection. L-deficient cardiovirus mutant (C19A/C22A) vs. Wild-type cardiovirus was evaluated on Apoptosis induction (cytochrome c efflux, caspase activation, DNA fragmentation). Infection with L-deficient cardiovirus mutants resulted in early caspase activation, cytochrome c efflux, and apoptosis, whereas wild-type virus elicited a strong antiapoptotic state.
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