Diverse Mechanisms Underlie Enhancement of Enteric Viruses by the Mammalian Intestinal Microbiota.

Katrina R. Grau,Alexa N. Roth,Stephanie M. Karst

doi:10.3390/v11080760

Abstract

Over the past two decades, there has been tremendous progress in understanding the impact of the intestinal microbiota on mammalian metabolism, physiology, and immune development and function. There has also been substantial advancement in elucidating the interplay between commensal and pathogenic bacteria. Relatively more recently, researchers have begun to investigate the effect of the intestinal microbiota on viral pathogenesis. Indeed, a growing body of literature has reported that commensal bacteria within the mammalian intestinal tract enhance enteric virus infections through a variety of mechanisms. Commensal bacteria or bacterial glycans can increase the stability of enteric viruses, enhance virus binding to host receptors, modulate host immune responses in a proviral manner, expand the numbers of host cell targets, and facilitate viral recombination. In this review, we will summarize the current literature exploring these effects of the intestinal microbiota on enteric virus infections.

Highlights

Enteric viruses infect the gastrointestinal (GI) tract following fecal-oral transmission and are collectively responsible for a tremendous disease burden
Two landmark studies published in Science in 2011 demonstrated that commensal bacteria stimulated poliovirus, reovirus, and mouse mammary tumor virus (MMTV) infections in the intestines of mice [24,25]: Mice treated with oral antibiotics prior to poliovirus infection had reduced viral shedding, decreased virus titers, and reduced disease severity compared to conventionally colonized mice, indicating that the intestinal microbiota facilitated poliovirus pathogenesis [25]
The intestinal microbiota is beneficial for the host in several aspects: Gut bacteria aid in host metabolism, gut motility, and nutrient uptake, maintain host physiology and homeostasis, help shape the host immune system, and protect against invading microorganisms

Summary

Introduction

Enteric viruses infect the gastrointestinal (GI) tract following fecal-oral transmission and are collectively responsible for a tremendous disease burden. They are often highly infectious and shed in significant quantities in the stool of infected individuals. Two landmark studies published in Science in 2011 demonstrated that commensal bacteria stimulated poliovirus, reovirus, and mouse mammary tumor virus (MMTV) infections in the intestines of mice [24,25]: Mice treated with oral antibiotics prior to poliovirus infection had reduced viral shedding, decreased virus titers, and reduced disease severity compared to conventionally colonized mice, indicating that the intestinal microbiota facilitated poliovirus pathogenesis [25]. Recent studies revealed that these viruses have evolved unique and varied strategies to exploit commensal microbes and enhance their efficiency at infecting mammalian hosts

Mechanisms of Bacterial Enhancement of Enteric Virus Infections

Bacterial Enhancement of Virus Attachment to Target Cells

Bacterial Modulation of Host Immunity in a Proviral Manner

Bacterial Promotion of Viral Recombination

Discussion and Future