Key result
Mutation variants of nonvirulent coxsackievirus B3 with nucleotide substitutions in the 5'-nontranslated region acquired high virulence, causing tissue destruction and severe mortality in vivo.
Nucleotide substitutions in the 5'-nontranslated region of nonvirulent CVB3 can lead to active virus replication and induce virulence.
Animal evidence links 5'UTR mutations to CVB3 virulence; leaves open relevance to human disease and requires clinical validation.
OBJECTIVE: To understand coxsackievirus B3 (CVB3) virulence at the molecular level. METHOD: A mutation library was generated from noncardiovirulent CVB3/0. Highly virulent mutation variants were recovered and characterized both phenotypically and genotypically. RESULTS: The variants consistently caused destruction of multiple tissues together with active virus production and induced severe mortality in vivo. The extent of infectious virus generation was directly correlated with that of histopathological aberration. Genotypic analysis of the entire genome indicated that the virulent viruses encode nucleotide substitutions in the 5'-nontranslated region, which have previously been identified in other virulent CVB3s. CONCLUSION: The present study provides evidence that particular nucleotide substitutions in the 5'-nontranslated region of nonvirulent CVB3 can lead to active virus replication, which is sufficient to induce virulence.
No takes yet. Share an insight, caveat, or question.
Seo et al. (2007) studied Coxsackievirus B3 (CVB3) infection. Mutation variants generated from noncardiovirulent CVB3/0 vs. Noncardiovirulent CVB3/0 was evaluated on Virulence phenotypes (tissue destruction, active virus production, and mortality in vivo). Mutation variants of nonvirulent coxsackievirus B3 with nucleotide substitutions in the 5'-nontranslated region acquired high virulence, causing tissue destruction and severe mortality in vivo.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: