Bacterial Lipopolysaccharide Binding Enhances Virion Stability and Promotes Environmental Fitness of an Enteric Virus

Robinson, C. M.; Jesudhasan, Palmy R.; Pfeiffer, Julie K.

doi:10.1016/j.chom.2013.12.004

Cited by 282 publications

(395 citation statements)

References 42 publications

(55 reference statements)

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“…Alternatively, there could be a coreceptor for RV-C that interacts with CDHR3, or a cofactor that facilitates binding and entry. For example, bacterial surface polysaccharides stabilize polioviruses and facilitate cell attachment by increasing binding to the viral receptor (33,34). In any case, experiments in our laboratory and elsewhere demonstrated that the RV-C interaction with native HeLa cells or other cell lines (e.g., A549) is not sufficient for efficient virus entry and replication (5,6,35).…”

Section: Discussionmentioning

confidence: 94%

Cadherin-related family member 3, a childhood asthma susceptibility gene product, mediates rhinovirus C binding and replication

Bochkov¹,

Watters

Ashraf³

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

371

345

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Members of rhinovirus C (RV-C) species are more likely to cause wheezing illnesses and asthma exacerbations compared with other rhinoviruses. The cellular receptor for these viruses was heretofore unknown. We report here that expression of human cadherin-related family member 3 (CDHR3) enables the cells normally unsusceptible to RV-C infection to support both virus binding and replication. A coding single nucleotide polymorphism (rs6967330, C529Y) was previously linked to greater cell-surface expression of CDHR3 protein, and an increased risk of wheezing illnesses and hospitalizations for childhood asthma. Compared with wild-type CDHR3, cells transfected with the CDHR3-Y529 variant had about 10-fold increases in RV-C binding and progeny yields. We developed a transduced HeLa cell line (HeLa-E8) stably expressing CDHR3-Y529 that supports RV-C propagation in vitro. Modeling of CDHR3 structure identified potential binding sites that could impact the virus surface in regions that are highly conserved among all RV-C types. Our findings identify that the asthma susceptibility gene product CDHR3 mediates RV-C entry into host cells, and suggest that rs6967330 mutation could be a risk factor for RV-C wheezing illnesses.

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Section: Discussionmentioning

confidence: 94%

Cadherin-related family member 3, a childhood asthma susceptibility gene product, mediates rhinovirus C binding and replication

Bochkov¹,

Watters

Ashraf³

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

371

345

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show abstract

“…Depletion of commensal bacteria by antibiotics inhibits poliovirus replication and pathogenesis in mice [147], although this was not seen in human infants given therapeutic doses of azithromycin [28]. It has also been observed in vitro that poliovirus infectivity is enhanced by exposure to bacterial surface polysaccharides such as lipopolysaccharide and peptidoglycan [147], possibly via the effect of these polysaccharides on virion stability and receptor attachment [148]. Analogous effects have been reported for rotavirus, which exhibits reduced infectivity and pathogenicity (but greater immunogenicity) in antibiotic-treated mice [149].…”

mentioning

confidence: 98%

Causes of Impaired Oral Vaccine Efficacy in Developing Countries

et al. 2017

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Oral vaccines are less immunogenic when given to infants in low-income compared with high-income countries, limiting their potential public health impact. Here, we review factors that might contribute to this phenomenon, including transplacental antibodies, breastfeeding, histo blood group antigens, enteric pathogens, malnutrition, microbiota dysbiosis and environmental enteropathy. We highlight several clear risk factors for vaccine failure, such as the inhibitory effect of enteroviruses on oral poliovirus vaccine. We also highlight the ambiguous and at times contradictory nature of the available evidence, which undoubtedly reflects the complex and interconnected nature of the factors involved. Mechanisms responsible for diminished immunogenicity may be specific to each oral vaccine. Interventions aiming to improve vaccine performance may need to reflect the diversity of these mechanisms. Enteric pathogens are a substantial threat to public health. This threat takes many forms, from the toxin-producing bacteria (e.g., Vibrio cholerae) and flagellated protozoa (e.g., Giardia lamblia) that colonize the mucosal surface of the small intestine to the enteroviruses that are capable of spreading via the bloodstream to the CNS, causing acute flaccid paralysis (e.g., poliovirus). Each year, enteric pathogens cause hundreds of millions of cases of diarrhea and approximately 800,000 deaths, the vast majority of which occur among children in low-income countries [1]. The most common causes of childhood diarrheal morbidity include rotavirus, Cryptosporidium, enterotoxigenic Escherichia coli and Shigella [2].Vaccines against enteric pathogens are important tools for mitigating this disease burden. Oral vaccines offer several distinct benefits compared with parenteral vaccines. They can be produced in large quantities at relatively low cost, are easy to administer and have the capacity to induce local immunity in the intestinal mucosa, thereby protecting vaccinated individuals against subsequent infection and -by blocking onward transmission -enhancing herd immunity [3,4]. Currently licensed oral vaccines include live-attenuated poliovirus vaccines containing one, two or three serotypes, live-attenuated rotavirus vaccines (Rotarix R , RotaTeq R , Lanzhou lamb rotavirus vaccine [China only] and Rotavac R [India only]), live-attenuated cholera vaccine (CVD 103-HgR or Vaxchora TM ), inactivated cholera vaccines (Dukoral R and Shanchol R ) and live-attenuated typhoid vaccine (Ty21a). Other oral vaccines are in development, including those against Shigella, enterotoxigenic E. coli, Campylobacter and Clostridium difficile, as well as several novel rotavirus vaccine candidates (including the human neonatal vaccine RV3-BB [5] and an oral bovine pentavalent vaccine [6]).Yet oral vaccines have an Achilles' heel -their immunogenicity and efficacy is impaired in low-income countries that experience the greatest burden of enteric disease (Box 1). For example, Rotarix has a 1-year protective efficacy against severe rotavirus-associated gas...

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“…Although we do not yet know the precise mechanism by which a HBGA (either free or bacterial-bound) stimulates HuNoV infection of B cells, we determined that it facilitates viral binding to the surface of B cells. Based on a previous study showing that LPS stimulates poliovirus binding to its receptor on permissive cells, 44 we speculate that the HBGA plays a similar role in bridging NoV attachment to a yet-to-be-identified entry receptor expressed on B cells.…”

Section: Commensal Bacteria Facilitate Norovirus Infectionsmentioning

confidence: 99%

Identification of a novel cellular target and a co-factor for norovirus infection – B cells & commensal bacteria

Karst

2015

Gut Microbes

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Bacterial Lipopolysaccharide Binding Enhances Virion Stability and Promotes Environmental Fitness of an Enteric Virus

Cited by 282 publications

References 42 publications

Cadherin-related family member 3, a childhood asthma susceptibility gene product, mediates rhinovirus C binding and replication

Cadherin-related family member 3, a childhood asthma susceptibility gene product, mediates rhinovirus C binding and replication

Causes of Impaired Oral Vaccine Efficacy in Developing Countries

Identification of a novel cellular target and a co-factor for norovirus infection – B cells & commensal bacteria

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