The influence of microbiota-derived metabolites on viral infections

Alwin, Ajisha; Karst, Stephanie M.

doi:10.1016/j.coviro.2021.05.006

Cited by 18 publications

(17 citation statements)

References 38 publications

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“…Cumulative evidence supports the view that microbial metabolites can regulate enteric viral infection [3][4][5]. Among them, bile acids (BAs) have been shown to play crucial roles in enhancing replication of enteric viruses such as porcine sapoviruses (PoSaV), porcine enteric calicivirus (PEC) and noroviruses (NoVs) [6][7][8]. The replication of PEC in the porcine kidney cell line LLC-PK1 is dependent on the presence of BAs in the culture medium for at least two reasons: 1) BAs facilitate PEC escape from the endosome into cytoplasm for initiation of viral replication [8]; 2) BAs inhibit cellular innate immunity by downregulating phosphorylation of signal transducer and activator of transcription 1 (STAT1) upon PEC infection in LLC-PK1 [9].…”

Section: Introductionmentioning

confidence: 92%

Bile acids promote the caveolae-associated entry of swine acute diarrhea syndrome coronavirus in porcine intestinal enteroids

Yang

Tang

et al. 2022

PLoS Pathog

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Intestinal microbial metabolites have been increasingly recognized as important regulators of enteric viral infection. However, very little information is available about which specific microbiota-derived metabolites are crucial for swine enteric coronavirus (SECoV) infection in vivo. Using swine acute diarrhea syndrome (SADS)-CoV as a model, we were able to identify a greatly altered bile acid (BA) profile in the small intestine of infected piglets by untargeted metabolomic analysis. Using a newly established ex vivo model–the stem cell-derived porcine intestinal enteroid (PIE) culture–we demonstrated that certain BAs, cholic acid (CA) in particular, enhance SADS-CoV replication by acting on PIEs at the early phase of infection. We ruled out the possibility that CA exerts an augmenting effect on viral replication through classic farnesoid X receptor or Takeda G protein-coupled receptor 5 signaling, innate immune suppression or viral attachment. BA induced multiple cellular responses including rapid changes in caveolae-mediated endocytosis, endosomal acidification and dynamics of the endosomal/lysosomal system that are critical for SADS-CoV replication. Thus, our findings shed light on how SECoVs exploit microbiome-derived metabolite BAs to swiftly establish viral infection and accelerate replication within the intestinal microenvironment.

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Section: Introductionmentioning

confidence: 92%

Bile acids promote the caveolae-associated entry of swine acute diarrhea syndrome coronavirus in porcine intestinal enteroids

Yang

Tang

et al. 2022

PLoS Pathog

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“…DAT is a product of commensal bacteria degradation of plant-derived polyphenol compounds (flavonoids) [ 63 ]. Administration of DAT into mice infected with influenza A virus protected mice from infection-associated mortality and morbidity but did not reduce viral titers [ 52 ].…”

Section: Potential Mechanisms Underlying Gut Microbiota–ifn–viral Int...mentioning

confidence: 99%

Microbiota regulation of viral infections through interferon signaling

Wirusanti

Baldridge

Harris

2022

Trends in Microbiology

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“…Overall, the literature lacks reports of protective effects of secondary metabolites synthesized de novo by members of the microbiota that exhibit antiviral activity. The role of SCFAs on viral infections has been reviewed elsewhere ( 145 ).…”

Section: Antiviral Moleculesmentioning

confidence: 99%

Microbial metabolites: cause or consequence in gastrointestinal disease?

Fobofou

Savidge

2022

American Journal of Physiology-Gastrointestinal and Liver Physi

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Systems biology studies have established that changes in gastrointestinal microbiome composition and function can adversely impact host physiology. Notable diseases synonymously associated with dysbiosis include inflammatory bowel diseases, cancers, metabolic disorders, opportunistic and recurrent pathogen infections. However, there is a scarcity of mechanistic data that advances our understanding of taxonomic correlations with pathophysiologic host-microbiome interactions. Generally, in order to survive a hostile gut environment, microbes are highly metabolically active and produce trans-kingdom signaling molecules to interact with competing microorganisms and the host. These specialized metabolites likely play important homeostatic roles and identifying disease-specific taxa and their effector pathways can provide better strategies for diagnosis, treatment, and prevention, as well as the discovery of innovative therapeutics. The signaling role of microbial biotransformation products such as bile acids, short chain fatty acids, polysaccharides and dietary tryptophan is increasingly recognized, but little is known about the identity and function of metabolites that are synthetized by microbial biosynthetic gene clusters. Here we consider how bioactive natural products directly encoded by the human microbiome can contribute to the pathophysiology of gastrointestinal disease, cancer, autoimmune, antimicrobial-resistant bacterial and viral infections (including COVID-19). We also present strategies used to discover these compounds and the biological activities they exhibit, with consideration of therapeutic interventions that could emerge from understanding molecular causation in gut microbiome research.

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The influence of microbiota-derived metabolites on viral infections

Cited by 18 publications

References 38 publications

Bile acids promote the caveolae-associated entry of swine acute diarrhea syndrome coronavirus in porcine intestinal enteroids

Bile acids promote the caveolae-associated entry of swine acute diarrhea syndrome coronavirus in porcine intestinal enteroids

Microbiota regulation of viral infections through interferon signaling

Microbial metabolites: cause or consequence in gastrointestinal disease?

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