Abstract
The presence of commensal bacteria enhances both acute and persistent infection of murine noroviruses. For several enteric viral pathogens, mechanisms by which these bacteria enhance infection involve direct interactions between the virus and bacteria. While it has been demonstrated that human noroviruses bind to a variety of commensal bacteria, it is not known if this is also true for murine noroviruses. The goal of this study was to characterize interactions between murine noroviruses and commensal bacteria and determine the impact of bacterial growth conditions, incubation temperature and time, on murine norovirus attachment to microbes that comprise the mammalian microbiome. We show that murine noroviruses bind directly to commensal bacteria and show similar patterns of attachment as human norovirus VLPs examined under the same conditions. Furthermore, while binding levels are not impacted by the growth phase of the bacteria, they do change with time and incubation temperature. We also found that murine norovirus can bind to a commensal fungal species, Candida albicans.
Highlights
Human noroviruses (HNoVs) are the leading cause of gastrointestinal illness worldwide, responsible for 685 million infections each year [1]
It has been previously demonstrated that human noroviruses bind to a variety of commensal bacteria [24], we set out to determine if murine noroviruses are capable of this wide-spread bacterial attachment
When choosing our panel of bacteria, we selected representative species of the phyla Bacteroidetes and Firmicutes (B. dorei and Lactobacillus spp., respectively) as these are the predominant phyla of the mammalian gut
Summary
Human noroviruses (HNoVs) are the leading cause of gastrointestinal illness worldwide, responsible for 685 million infections each year [1]. HNoVs are estimated to cause 200,000 deaths in children under 5 years of age and are increasingly associated with devastating infections in immunocompromised hosts [3,4,5,6]. Despite this large disease burden, relatively little is known about the pathogenesis of this virus.
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