TY - JOUR
T1 - Bacterial lipopolysaccharide binding enhances virion stability and promotes environmental fitness of an enteric virus
AU - Robinson, Christopher M.
AU - Jesudhasan, Palmy R.
AU - Pfeiffer, Julie K.
N1 - Funding Information:
We thank Gavin Best and Pamela de la Cruz for assistance with experiments, Satoshi Koike for mice, Stanley Lemon for advice on PaSTRy experiments, and Andrea Erickson and John Schoggins for comments on the manuscript. This work was funded by the World Health Organization Global Polio Eradication Initiative (J.K.P.), a Burroughs Wellcome Fund Investigator in the Pathogenesis of Infectious Disease award (J.K.P.), R01 AI74668 (J.K.P.), a Hartwell Foundation postdoctoral fellowship (C.M.R.), and T32 AI007520 (C.M.R.).
PY - 2014/1/15
Y1 - 2014/1/15
N2 - Summary 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.
AB - Summary 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.
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U2 - 10.1016/j.chom.2013.12.004
DO - 10.1016/j.chom.2013.12.004
M3 - Article
C2 - 24439896
AN - SCOPUS:84892621089
SN - 1931-3128
VL - 15
SP - 36
EP - 46
JO - Cell Host and Microbe
JF - Cell Host and Microbe
IS - 1
ER -