Intestinal Microbiota and Susceptibility to Viral Infections

Monedero, Vicente; Rodrı́guez-Dı́az, Jesús

doi:10.1016/b978-0-12-802189-7.00062-9

Cited by 4 publications

(4 citation statements)

References 73 publications

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“…Similar to IBD, for example, probiotics protect the host from viral infection by modulating the composition of the gut microbiota, enhancing intestinal barrier function, and promoting mucosal immunity (Peña-Gil et al, 2021 ). Additionally, they interfere with the binding of viruses to target cells by blocking viral receptors and binding to the surface in a competitive rejection manner, facilitating their excretion in the feces (Monedero and Rodríguez-Díaz, 2016 ). Furthermore, the presence of Bifidobacterium adolescentis inhibits the attachment of NoV GI.1 VLPs to epithelial cells in vitro (Li et al, 2016 ).…”

Section: Fut2 Gene and Susceptibility To Nov And Rv Infectionsmentioning

confidence: 99%

Fucosyltransferase 2: A Genetic Risk Factor for Intestinal Diseases

Zhang

et al. 2022

Front. Microbiol.

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The fucosyltransferase 2 gene (FUT2) mediates the synthesis of histoblood group antigens (HBGA) that occur in vivo from multiple organs, particularly on the surface of intestinal epithelial cells and body fluids. To date, many studies have demonstrated that the interaction of HBGA with the host microbiota is the cause of pathogenesis of intestinal diseases, making FUT2 non-secretor a risk factor for inflammatory bowel disease (IBD) due to the lack of HBGA. As HBGA also acts as an attachment site for norovirus (NoV) and rotavirus (RV), the non-secretor becomes a protective factor for both viral infections. In addition, the interaction of norovirus and rotavirus with symbiotic bacteria has been found to play an important role in regulating enteroviral infection in IBD. Given the current incomplete understanding of the complex phenomenon and the underlying pathogenesis of intestinal diseases such as IBD, it has recently been hypothesized that the FUT2 gene regulates intestinal bacteria through attachment sites, may help to unravel the role of FUT2 and intestinal flora in the mechanism of intestinal diseases in the future, and provide new ideas for the prevention and treatment of intestinal diseases through more in-depth studies.

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Section: Fut2 Gene and Susceptibility To Nov And Rv Infectionsmentioning

confidence: 99%

Fucosyltransferase 2: A Genetic Risk Factor for Intestinal Diseases

Zhang

et al. 2022

Front. Microbiol.

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“…Probiotics protect the host from viral infection by modulating gut microbiota composition, enhancing intestinal barrier function, and promoting mucosal immunity [70]. Additionally, they interfere with the binding of the virus to their target cells by competitive exclusion by blocking viral receptors and binding viruses on the surface to promote their elimination in faeces [71].…”

Section: Bacteria Against Enteric Viral Infectionsmentioning

confidence: 99%

The Role of Host Glycobiology and Gut Microbiota in Rotavirus and Norovirus Infection, an Update

Peña-Gil

Santiso-Bellón

Gozalbo-Rovira

et al. 2021

IJMS

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Rotavirus (RV) and norovirus (NoV) are the leading causes of acute gastroenteritis (AGE) worldwide. Several studies have demonstrated that histo-blood group antigens (HBGAs) have a role in NoV and RV infections since their presence on the gut epithelial surfaces is essential for the susceptibility to many NoV and RV genotypes. Polymorphisms in genes that code for enzymes required for HBGAs synthesis lead to secretor or non-secretor and Lewis positive or Lewis negative individuals. While secretor individuals appear to be more susceptible to RV infections, regarding NoVs infections, there are too many discrepancies that prevent the ability to draw conclusions. A second factor that influences enteric viral infections is the gut microbiota of the host. In vitro and animal studies have determined that the gut microbiota limits, but in some cases enhances enteric viral infection. The ways that microbiota can enhance NoV or RV infection include virion stabilization and promotion of virus attachment to host cells, whereas experiments with microbiota-depleted and germ-free animals point to immunoregulation as the mechanism by which the microbiota restrict infection. Human trials with live, attenuated RV vaccines and analysis of the microbiota in responder and non-responder individuals also allowed the identification of bacterial taxa linked to vaccine efficacy. As more information is gained on the complex relationships that are established between the host (glycobiology and immune system), the gut microbiota and intestinal viruses, new avenues will open for the development of novel anti-NoV and anti-RV therapies.

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“…Several studies demonstrate the beneficial effect of probiotic bacteria against enteric virus infections and many other diseases [66][67][68][69]. Probiotics protect the host from viral infection by modulating gut microbiota composition, enhancing intestinal barrier function and promoting mucosal immunity [70], as well as interfering with the binding of virus to their target cells by competitive exclusion by blocking viral receptors and binding viruses on the surface to promote their elimination in faeces [71].…”

Section: Bacteria Against Enteric Viral Infectionsmentioning

confidence: 99%

The Role of Host Glycobiology and Gut Microbiota in Rotavirus and Norovirus Infection, an Update

Peña-Gil¹,

Santiso-Bellón²,

Gozalbo-Rovira³

et al. 2021

Preprint

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Rotavirus (RV) and norovirus (NoV) are the leading cause of acute gastroenteritis (AGE) worldwide. Several studies have demonstrated that histo-blood group antigens (HBGAs) have a role in NoV and RV infections, since their presence on the gut epithelial surfaces is essential for the susceptibility to many NoV and RV genotypes. Polymorphisms in genes that code for enzymes required for HBGAs synthesis lead to secretor or non-secretor and Lewis positive and Lewis negative individuals. While secretor individuals appear to be more susceptible to RV infections, regarding NoVs infections there are too many discrepancies that prevent drawing conclusions. A second factor that influences enteric viral infections is the gut microbiota of the host. In vitro and animal studies have determined that the gut microbiota limits, but in some cases enhances, enteric viral infection. The ways microbiota can enhance NoV or RV infection include virion stabilization and promotion of virus attachment to host cells, whereas experiments with microbiota-depleted and germ-free animals point to immunoregulation as the mechanism by which the microbiota restricts infection. Human trials with live, attenuated RV vaccines and analysis of the microbiota in responders and non-responders individuals also allowed the identification of bacterial taxa linked to vaccine efficacy. As more information is gained on the complex relationships that are established between the host (glycobiology and immune system), the gut microbiota and the intestinal viruses, new avenues will be open for the development of novel anti-NoV and anti-RV therapies.

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Intestinal Microbiota and Susceptibility to Viral Infections

Cited by 4 publications

References 73 publications

Fucosyltransferase 2: A Genetic Risk Factor for Intestinal Diseases

Fucosyltransferase 2: A Genetic Risk Factor for Intestinal Diseases

The Role of Host Glycobiology and Gut Microbiota in Rotavirus and Norovirus Infection, an Update

The Role of Host Glycobiology and Gut Microbiota in Rotavirus and Norovirus Infection, an Update

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