Norwalk virus binds to histo-blood group antigens present on gastroduodenal epithelial cells of secretor individuals

Marionneau, Séverine; Ruvoën, Nathalie; Moullac-Vaidye, Béatrice Le; Clément, Michel; Cailleau-Thomas, Anne; Ruiz–Palacois, Guillermo; Huang, Pengwei; Jiang, Xi; Pendu, Jacques Le

doi:10.1053/gast.2002.33661

Cited by 455 publications

(465 citation statements)

References 43 publications

(40 reference statements)

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“…Consistent with this, HuNoVs can be internalized by enterocytes in culture [30][31][32] and MuNoVs can be transcytosed across a confluent epithelial monolayer to target underlying permissive macrophages 33 ; in all of these studies, no evidence of viral replication in the enterocytes themselves was noted. Indeed, we confirmed that the GII.4-Sydney HuNoV could cross a confluent intestinal epithelial monolayer to infect underlying B cells in the basal chamber of a transwell system.…”

Section: A Gii4-sydney Human Norovirus Infects B Cells In Vitromentioning

confidence: 72%

“…Because we used unprocessed stool as a source of virus, we reasoned that the most likely candidate for a filterable co-factor was commensal bacteria. In selecting a specific commensal bacteria to test for stimulatory activity, we were guided by the knowledge that HuNoVs bind HBGAs in a virus strainspecific manner 30,41 and that certain bacteria express glycans indistinguishable from human HBGAs. 42 In fact, Miura et al recently revealed that HBGAexpressing commensal bacteria such as Enterobacter cloacae can bind HuNoV VLPs.…”

Section: Commensal Bacteria Facilitate Norovirus Infectionsmentioning

confidence: 99%

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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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Section: A Gii4-sydney Human Norovirus Infects B Cells In Vitromentioning

confidence: 72%

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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“…In humans, genetic factors such as polymorphisms in the FUT1 (H), FUT2 (Se), and FUT3 (Le) genes that code for glycosyltransferases responsible for producing carbohydrate chains have been associated with susceptibility to NoV GI and II (23,26,27). At present we are evaluating reagents and assays to test for HBGA in pigs to ascertain if the same or similar genetic factors influence NoV infection of Gn pigs.…”

Section: Discussionmentioning

confidence: 99%

Pathogenesis of a Genogroup II Human Norovirus in Gnotobiotic Pigs

Cheetham

Souza

Meulia

et al. 2006

J Virol

255

264

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Human noroviruses (HuNoVs) are a major cause of foodborne gastroenteritis worldwide. Because they do not grow in cell culture and there is no animal model for HuNoVs, pathogenesis studies have been hampered. Thus, little is known about their replication strategies or induction of neutralizing antibodies.The limited information on their pathogenesis is from human volunteer studies of HuNoV infections in which villus atrophy in duodenal biopsies and presence of malabsorptive diarrhea were described (1,7,8). No information is available on lesions in other portions of the intestines of these volunteers (9). Intestinal transplant pediatric patients that were diagnosed with HuNoV infection developed secretory or osmotic diarrhea (19,20,31). These patients had prolonged diarrhea (17 to 326 days) due to immunosuppressive therapy. The detection of HuNoV RNA and the clinical symptoms remitted after reduction of the immunosuppressive therapy. Usually in exposed individuals, histologic lesions correlate with diarrhea, but in one report, lesions in volunteers who did not show clinical symptoms were described (42). There are also numerous reports of asymptomatic individuals who were infected with HuNoVs and shed virus in the feces (11, 28).Most past attempts to study these viruses in an animal model may have failed because (i) the human strains that were used were not closely related to the host animal NoV strains, (ii) sensitive detection techniques were lacking, and finally (iii) the role of histo-blood group antigen (HBGA) phenotypes in differential susceptibility of the host was unrecognized. Our goal was to adapt a HuNoV strain to replicate in the gnotobiotic (Gn) pig to develop an animal model for the study of HuNoV pathogenesis. Gnotobiotic pigs are good models for human enteric diseases (40) because pigs resemble humans in their gastrointestinal anatomy, physiology, and immune responses. The Gn pigs are immunocompetent at birth, but they lack maternal antibodies and previous or ongoing exposure to microbial agents, including caliciviruses.Recently, viral RNA genetically similar to that of human NoV GII (65 to 71% amino acid sequence identity in the capsid gene) was detected in pigs in Japan (46, 47) and Europe (22,48). In U.S. swine, our laboratory detected both viral RNA and virus particles similar to GII HuNoV (70% sequence identity in the capsid region) which were infectious for Gn pigs (50). Our approach to infect Gn pigs with a HuNoV was to use a GII strain that is closely related genetically to the identified GII porcine NoVs and that has a broad HBGA binding pattern because little information or reagents are available for pig HBGA. Additionally, we used sensitive assays and reagents including reverse transcription (RT)-PCR to detect fecal shedding, virus-like particles (VLPs) for serological assays, and antisera to these VLPs for antigen enzyme-linked immunosor-

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“…The third and last case we will consider here is autosomal recessive fucosyltransferase 2 (FUT2) deficiency, which was discovered in 2003. Individuals with this deficiency are naturally resistant to diarrhea caused by noroviruses (8,9). This condition is typically benign in the developed world today but would have been potentially lifethreatening in ancient times, as it still is in developing countries.…”

Section: Other Forms Of Mendelian Resistance To Infectionmentioning

confidence: 99%

Severe infectious diseases of childhood as monogenic inborn errors of immunity

Casanova

2015

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

201

163

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This paper reviews the developments that have occurred in the field of human genetics of infectious diseases from the second half of the 20th century onward. In particular, it stresses and explains the importance of the recently described monogenic inborn errors of immunity underlying resistance or susceptibility to specific infections. The monogenic component of the genetic theory provides a plausible explanation for the occurrence of severe infectious diseases during primary infection. Over the last 20 y, increasing numbers of life-threatening infectious diseases striking otherwise healthy children, adolescents, and even young adults have been attributed to single-gene inborn errors of immunity. These studies were inspired by seminal but neglected findings in plant and animal infections. Infectious diseases typically manifest as sporadic traits because human genotypes often display incomplete penetrance (most genetically predisposed individuals remain healthy) and variable expressivity (different infections can be allelic at the same locus). Infectious diseases of childhood, once thought to be archetypal environmental diseases, actually may be among the most genetically determined conditions of mankind. This nascent and testable notion has interesting medical and biological implications.

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Norwalk virus binds to histo-blood group antigens present on gastroduodenal epithelial cells of secretor individuals

Abstract: rNV VLPs use H type 1 and/or H types (3/4) as ligands on gastroduodenal epithelial cells of secretor individuals.

Cited by 455 publications

References 43 publications

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

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

Pathogenesis of a Genogroup II Human Norovirus in Gnotobiotic Pigs

Severe infectious diseases of childhood as monogenic inborn errors of immunity

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