Enterovirus 71 (EV71) which causes mild illness in children is also associated with severe neurological complications. This study analyzed the complete genomes of EV71 strains derived from mild and severe diseases in order to determine whether the differences of EV71 genomes were responsible for different clinical presentations. Compared to complete genomes of EV71 strains derived from mild cases (less virulent strains), nucleotide differences in EV71 strains isolated from severe cases (more virulent strains) were observed primarily in the internal ribosomal entry site (IRES) of the 5′‐untranslated region (UTR), which is vital for the cap‐independent translation of viral proteins. In the protein‐coding region, an E–Q substitution at amino acid position 145 of structural protein VP1 that occurred in more than one of more virulent strains was observed. This site is known to be related functionally to receptor binding and virulence in mice. Overall, strains (Group III) isolated from patients with fatal or severe sequelae outcomes had greater sequence substitutions in the 5′‐UTR and/or protein‐coding region and exhibited a relatively low‐average homology to less virulent strains across the entire genome, indicating the possibility of significant genomic diversity in the most virulent EV71 strains. Further studies of EV71 pathogenesis should examine the significance of genomic diversity and the effects of multiple mutations in a viral population. J. Med. Virol. 84:931–939, 2012. © 2012 Wiley Periodicals, Inc.

The prevalence of vancomycin resistant enterococcus (VRE) carrier-state has been increasing in patients of intensive care unit and it would be a public health threat. Different research groups conducted decolonizing VRE with probiotic and the results were controversial. Therefore, a systemic approach to search for the probiotic species capable of decolonizing VRE is necessary. Thus, VRE was co-cultured with ten probiotic species. The fluctuations of each bacterial population were analyzed by 16S rRNA sequencing. Microbial network analysis (MNA) was exploited to identify the most critical species in inhibiting the VRE population. The MNA-selected probiotic cocktail was then validated for its efficacy in inhibiting VRE, decolonizing VRE from Caco-2 cells via three approaches: exclusion, competition, and displacement. Finally, the expression of VRE virulence genes after co-incubation with the probiotic cocktail were analyzed with quantitative real-time PCR (qRT-PCR). The MNA-selected probiotic cocktail includes Bacillus coagulans, Lactobacillus rhamnosus GG, Lactobacillus reuteri, and Lactobacillus acidophilus. This probiotic combination significantly reduces the population of co-cultured VRE and prevents VRE from binding to Caco-2 cells by down-regulating several host-adhesion genes of VRE. Our results suggested the potential of this four-strain probiotic cocktail in clinical application for the decolonization of VRE in human gut.