Pathogenesis, Immunity and the Role of Microbiome/Probiotics in Enteric Virus Infections in Humans and Animal Models

The gut microbiota has a profound impact on the resistance, pathogenesis, and immunity of enteric viral pathogens. Commensal microbes may prevent the host from infection or enhance infection by altering virus stability, attachment or cellular entry. Additionally, microbiota members can stimulate or suppress host immune responses to the viral infection. In most cases, the gut microbiota plays a role in host resistance against invading enteric viral pathogens; hence, germ-free animals are more susceptible to infection of various enteric pathogens. However, increasing evidence has demonstrated that certain commensal bacteria can enhance enteric viral infection. Exact mechanisms by which specific bacteria carry out these effects are not clearly understood in most instances. In this chapter, human norovirus (HuNoV) and human rotavirus (HRV), the two most important viral pathogens causing gastroenteritis, are chosen for the discussion of the impacts and mechanisms of microbiome–host interactions on viral gastroenteritis. The pathogenesis and immunity of HuNoV and HRV in humans and in germ-free animal models, particularly gnotobiotic (Gn) mice and pigs, and Gn pigs transplanted with human gut microbiota are reviewed. Findings from studies on host–microbiome interactions on the pathogenesis and immunity of the two viruses, and mechanisms of probiotics/prebiotics in ameliorating their infection and diseases, are summarized. Unraveling the role of microbiome and specific probiotics in the infectivity, pathogenesis, and immunity of HuNoV and HRV facilitates the development of strategies for manipulating the microbiome against viral infections. Further studies are needed to improve our understanding of mechanisms underlying host–microbiome interactions in the pathophysiology of enteric viral diseases.