Enteric viruses evoke broad host immune responses resembling those elicited by the bacterial microbiome

Dallari, Simone; Heaney, Thomas; Rosas-Villegas, Adriana; Neil, Jessica A.; Wong, Serre-Yu; Brown, Judy J.; Urbanek, Kelly; Herrmann, Christin; Depledge, Daniel P.; Dermody, Terence S.; Cadwell, Ken

doi:10.1016/j.chom.2021.03.015

Cited by 41 publications

(30 citation statements)

References 114 publications

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“…Norovirus is therefore sufficient to preserve gut homeostasis and intestinal immunity in a manner that is typically served by microbiota. With potential for such an influential impact, it should be no surprise that alterations and dysbiosis in the viral composition have been associated with several diseases and can alter host immune homeostasis, particularly within mucosal environments (142,144).…”

Section: Virome As a Contributor To Host Immunity And Microbial Regulationmentioning

confidence: 99%

“…An exhaustive study by Dallari et al characterized host immune responses to several asymptomatic virus infections (acute and persistent strains of MNV, mastadenoviruses, astrovirus, parvoviruses, and reoviruses) in conventional and germ-free mice (144). The authors identified both distinct and common immune modulation contributed by viral and bacterial microbes.…”

Section: Immune Regulation By Commensal Virusesmentioning

confidence: 99%

“…There is a significant degree of bidirectional influence between the microbiome and antiviral response. Not only does infection alter the microbial homeostasis, but the microbiome can also have a significant impact on the outcome of virus infection and the ensuing immunological responses (144,(166)(167)(168). The microbiome has been shown to determine severity of viral infection and promote resistance to enteric infection (169)(170)(171).…”

Section: Intestinal Commensal Bacteria Can Influence Virus Outcomesmentioning

confidence: 99%

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Virus Infection Is an Instigator of Intestinal Dysbiosis Leading to Type 1 Diabetes

Morse

Horwitz

2021

Front. Immunol.

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In addition to genetic predisposition, environmental determinants contribute to a complex etiology leading to onset of type 1 diabetes (T1D). Multiple studies have established the gut as an important site for immune modulation that can directly impact development of autoreactive cell populations against pancreatic self-antigens. Significant efforts have been made to unravel how changes in the microbiome function as a contributor to autoimmune responses and can serve as a biomarker for diabetes development. Large-scale longitudinal studies reveal that common environmental exposures precede diabetes pathology. Virus infections, particularly those associated with the gut, have been prominently identified as risk factors for T1D development. Evidence suggests recent-onset T1D patients experience pre-existing subclinical enteropathy and dysbiosis leading up to development of diabetes. The start of these dysbiotic events coincide with detection of virus infections. Thus viral infection may be a contributing driver for microbiome dysbiosis and disruption of intestinal homeostasis prior to T1D onset. Ultimately, understanding the cross-talk between viral infection, the microbiome, and the immune system is key for the development of preventative measures against T1D.

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Section: Virome As a Contributor To Host Immunity And Microbial Regulationmentioning

confidence: 99%

Section: Immune Regulation By Commensal Virusesmentioning

confidence: 99%

Section: Intestinal Commensal Bacteria Can Influence Virus Outcomesmentioning

confidence: 99%

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Virus Infection Is an Instigator of Intestinal Dysbiosis Leading to Type 1 Diabetes

Morse

Horwitz

2021

Front. Immunol.

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“…We will focus our attention primarily on the effects of gut bacteria on host physiology. However, it is increasingly clear that intestinal fungi, viruses, archaea, and other eukaryotic species can profoundly impact host phenotypes, such as promoting intestinal immune system maturation and regulating disease susceptibility, often able to imprint phenotypic responses equivalent to gut bacteria ( Kernbauer et al, 2014 ; Chudnovskiy et al, 2016 ; Escalante et al, 2016 ; Lin et al, 2020 ; Yeung et al, 2020 ; Dallari et al, 2021 ). Moreover, these agents do not act in isolation, and their direct or indirect interactions may regulate host health as has been demonstrated in murine models of inflammatory bowel disease (IBD) and parasitic infection ( Cadwell et al, 2010 ; Hayes et al, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

Controlled Complexity: Optimized Systems to Study the Role of the Gut Microbiome in Host Physiology

Glowacki

Engelhart

2021

Front. Microbiol.

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The profound impact of the gut microbiome on host health has led to a revolution in biomedical research, motivating researchers from disparate fields to define the specific molecular mechanisms that mediate host-beneficial effects. The advent of genomic technologies allied to the use of model microbiomes in gnotobiotic mouse models has transformed our understanding of intestinal microbial ecology and the impact of the microbiome on the host. However, despite incredible advances, our understanding of the host-microbiome dialogue that shapes host physiology is still in its infancy. Progress has been limited by challenges associated with developing model systems that are both tractable enough to provide key mechanistic insights while also reflecting the enormous complexity of the gut ecosystem. Simplified model microbiomes have facilitated detailed interrogation of transcriptional and metabolic functions of the microbiome but do not recapitulate the interactions seen in complex communities. Conversely, intact complex communities from mice or humans provide a more physiologically relevant community type, but can limit our ability to uncover high-resolution insights into microbiome function. Moreover, complex microbiomes from lab-derived mice or humans often do not readily imprint human-like phenotypes. Therefore, improved model microbiomes that are highly defined and tractable, but that more accurately recapitulate human microbiome-induced phenotypic variation are required to improve understanding of fundamental processes governing host-microbiome mutualism. This improved understanding will enhance the translational relevance of studies that address how the microbiome promotes host health and influences disease states. Microbial exposures in wild mice, both symbiotic and infectious in nature, have recently been established to more readily recapitulate human-like phenotypes. The development of synthetic model communities from such “wild mice” therefore represents an attractive strategy to overcome the limitations of current approaches. Advances in microbial culturing approaches that allow for the generation of large and diverse libraries of isolates, coupled to ever more affordable large-scale genomic sequencing, mean that we are now ideally positioned to develop such systems. Furthermore, the development of sophisticated in vitro systems is allowing for detailed insights into host-microbiome interactions to be obtained. Here we discuss the need to leverage such approaches and highlight key challenges that remain to be addressed.

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“…Nonetheless, like most wildlife studies, our work offers a snapshot perspective of ongoing parasitic challenges with no knowledge of exposure to parasites throughout an individual's lifetime. Previous infections can modify the immune environment of the host [100,101], for instance by affecting the Th1-Th2 balance [102,103] or by shifting the availability of microbial metabolic compounds [104,105], with a knock-on effect on susceptibility to infection. Moreover, a history of infection co-occurrence in helminth-mice models have been shown to influence immunity to invading parasites even after helminth clearance [102,106].…”

Section: Plos Pathogensmentioning

confidence: 99%

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Enteric viruses evoke broad host immune responses resembling those elicited by the bacterial microbiome

Cited by 41 publications

References 114 publications

Virus Infection Is an Instigator of Intestinal Dysbiosis Leading to Type 1 Diabetes

Virus Infection Is an Instigator of Intestinal Dysbiosis Leading to Type 1 Diabetes

Controlled Complexity: Optimized Systems to Study the Role of the Gut Microbiome in Host Physiology

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