Key result
Mutational disruption of the uridylylating CRE(2C) in Coxsackievirus B3 significantly suppresses replication and drives the de novo generation of 5'-terminal genomic deletions.
Coxsackievirus B3 can replicate without a uridylylating CRE(2C), though at a significantly reduced rate, leading to error-prone priming and 5'-terminal genomic deletions.
No takes yet. Share an insight, caveat, or question.
May guide CVB3 attenuation strategies in myocarditis models; leaves open clinical translation and therapeutic utility.
Smithee et al. (2015) studied Coxsackievirus B3 infection. Mutational disruption of cis-acting replication element 2C [CRE(2C)] vs. Wild-type CVB3 was evaluated on Viral replication and generation of genomic deletions. Mutational disruption of the uridylylating CRE(2C) in Coxsackievirus B3 significantly suppresses replication and drives the de novo generation of 5'-terminal genomic deletions.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: