Bacterial lipopolysaccharide binding enhances virion stability and promotes environmental fitness of an enteric virus

Cell Host Microbe. 2014 Jan 15;15(1):36-46. doi: 10.1016/j.chom.2013.12.004.


Enteric viruses, including poliovirus and reovirus, encounter a vast microbial community in the mammalian gastrointestinal tract, which has been shown to promote virus replication and pathogenesis. Investigating the underlying mechanisms, we find that poliovirus binds bacterial surface polysaccharides, which enhances virion stability and cell attachment by increasing binding to the viral receptor. Additionally, we identified a poliovirus mutant, VP1-T99K, with reduced lipopolysaccharide (LPS) binding. Although T99K and WT poliovirus cell attachment, replication, and pathogenesis in mice are equivalent, VP1-T99K poliovirus was unstable in feces following peroral inoculation of mice. Consequently, the ratio of mutant virus in feces is reduced following additional cycles of infection in mice. Thus, the mutant virus incurs a fitness cost when environmental stability is a factor. These data suggest that poliovirus binds bacterial surface polysaccharides, enhancing cell attachment and environmental stability, potentially promoting transmission to a new host.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Feces / virology
  • Fibroblasts / virology
  • Genetic Fitness / physiology
  • HeLa Cells
  • Host-Pathogen Interactions*
  • Humans
  • Lipopolysaccharides / metabolism*
  • Mice
  • Mice, Transgenic
  • Microbial Interactions / genetics*
  • Mutation
  • Poliomyelitis / metabolism
  • Poliomyelitis / mortality
  • Poliomyelitis / virology*
  • Poliovirus / genetics
  • Poliovirus / metabolism*
  • Poliovirus / pathogenicity
  • Protein Binding
  • Receptors, Virus / metabolism
  • Survival Analysis
  • Viral Plaque Assay
  • Virion / genetics
  • Virion / metabolism*
  • Virion / pathogenicity
  • Virus Attachment
  • Virus Replication


  • Lipopolysaccharides
  • Receptors, Virus