Inhibition of the interaction between the SARS-CoV Spike protein and its cellular receptor by anti-histo-blood group antibodies

Guillon, Patrice; Clément, Michel; Sébille, Véronique; Rivain, Jean Gérard; Chou, Chih Fong; Ruvoën-Clouet, Nathalie; Pendu, Jacques Le

doi:10.1093/glycob/cwn093

Cited by 363 publications

(463 citation statements)

References 30 publications

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“…Addition of anti-histo blood group NAbs was found to bind to these viruses and elicit antibody-mediated inactivation [59,60]. Further studies have investigated NAb-mediated viral neutralisation using other, analogous glycan structures, showing supporting results [61,62]. However, it is unlikely that nonsecretors develop NAbs with specificity to secretor glycans, as a(1,2)-fucosylated glycans exist in nonmucosal sites, which are not reliant on FUT2.…”

Section: Anti-sugar Antibodies: Host Antibodies Recognise Nonself Glymentioning

confidence: 94%

Infection’s Sweet Tooth: How Glycans Mediate Infection and Disease Susceptibility

Taylor

McGuckin

Wesselingh

et al. 2018

Trends in Microbiology

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Glycans form a highly variable constituent of our mucosal surfaces and profoundly affect our susceptibility to infection and disease. The diversity and importance of these surface glycans can be seen in individuals who lack a functional copy of the fucosyltransferase gene, FUT2. Representing around one-fifth of the population, these individuals have an altered susceptibility to many bacterial and viral infections and diseases. The mediation of host-pathogen interactions by mucosal glycans, such as those added by FUT2, is poorly understood. We highlight, with specific examples, important mechanisms by which host glycans influence infection dynamics, including by: acting as pathogen receptors (or receptor-decoys), promoting microbial stability, altering the physical characteristics of mucus, and acting as immunological markers. We argue that the effect glycans have on infection dynamics has profound implications for many aspects of healthcare and policy, including clinical management, outbreak control, and vaccination policy.

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Section: Anti-sugar Antibodies: Host Antibodies Recognise Nonself Glymentioning

confidence: 94%

Infection’s Sweet Tooth: How Glycans Mediate Infection and Disease Susceptibility

Taylor

McGuckin

Wesselingh

et al. 2018

Trends in Microbiology

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“…Severe acute respiratory syndrome (SARS) is caused by the SARS coronavirus (SARS-CoV), an RNA virus. The original SARS outbreak in the winter of 2002 to 2003 infected Ͼ8,000 individuals worldwide, with a fatality rate of 10% (292). Like other human coronaviruses, SARS-CoV infects the mucosal epithelium, causing an acute respiratory illness often accompanied by gastroenteritis.…”

Section: Sars and Abomentioning

confidence: 99%

Blood Groups in Infection and Host Susceptibility

2015

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SUMMARY Blood group antigens represent polymorphic traits inherited among individuals and populations. At present, there are 34 recognized human blood groups and hundreds of individual blood group antigens and alleles. Differences in blood group antigen expression can increase or decrease host susceptibility to many infections. Blood groups can play a direct role in infection by serving as receptors and/or coreceptors for microorganisms, parasites, and viruses. In addition, many blood group antigens facilitate intracellular uptake, signal transduction, or adhesion through the organization of membrane microdomains. Several blood groups can modify the innate immune response to infection. Several distinct phenotypes associated with increased host resistance to malaria are overrepresented in populations living in areas where malaria is endemic, as a result of evolutionary pressures. Microorganisms can also stimulate antibodies against blood group antigens, including ABO, T, and Kell. Finally, there is a symbiotic relationship between blood group expression and maturation of the gastrointestinal microbiome.

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“…Single-transfectant CHO cells that stably express the enzyme fucosyltransferase (Fut2) express the H antigen (Hϩ/AϪ/BϪ). Double-transfectant CHO cells expressing Fut2 and either A-type glycosyltransferase or B-type glycosyltransferase express the A antigen (Hϩ/Aϩ/BϪ) or B antigen (Hϩ/AϪ/Bϩ), respectively (28). Polylactosamines were assayed on CHO cells by flow cytometry using the biotinylated lectins STL from Solanum tuberculosum (potato; Biovalley), LEL from Lycospersum (tomato; Biovalley), and streptavidin-peridinin chlorophyll protein conjugate (BD Biosciences) at 1 g/ml.…”

Section: Comparison Of Vp8* Sequencesmentioning

confidence: 99%

The VP8* Domain of Neonatal Rotavirus Strain G10P[11] Binds to Type II Precursor Glycans

Ramani

Cortés-Penfield

et al. 2013

J Virol

Self Cite

118

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e Naturally occurring bovine-human reassortant rotaviruses with a P[11] VP4 genotype exhibit a tropism for neonates. Interaction of the VP8* domain of the spike protein VP4 with sialic acid was thought to be the key mediator for rotavirus infectivity. However, recent studies have indicated a role for nonsialylated glycoconjugates, including histo-blood group antigens (HBGAs), in the infectivity of human rotaviruses. We sought to determine if the bovine rotavirus-derived VP8* of a reassortant neonatal G10P[11] virus interacts with hitherto uncharacterized glycans. In an array screen of >600 glycans, VP8* P[11] showed specific binding to glycans with the Gal␤1-4GlcNAc motif, which forms the core structure of type II glycans and is the precursor of H type II HBGA. The specificity of glycan binding was confirmed through hemagglutination assays; GST-VP8* P[11] hemagglutinates type O, A, and B red blood cells as well as pooled umbilical cord blood erythrocytes. Further, G10P[11] infectivity was significantly enhanced by the expression of H type II HBGA in CHO cells. The bovine-origin VP4 was confirmed to be essential for this increased infectivity, using laboratory-derived reassortant viruses generated from sialic acid binding rotavirus SA11-4F and a bovine G10P[11] rotavirus, B223. The binding to a core glycan unit has not been reported for any rotavirus VP4. Core glycan synthesis is constitutive in most cell types, and modification of these glycans is thought to be developmentally regulated. These studies provide the first molecular basis for understanding neonatal rotavirus infections, indicating that glycan modification during neonatal development may mediate the agerestricted infectivity of neonatal viruses.

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Inhibition of the interaction between the SARS-CoV Spike protein and its cellular receptor by anti-histo-blood group antibodies

Cited by 363 publications

References 30 publications

Infection’s Sweet Tooth: How Glycans Mediate Infection and Disease Susceptibility

Infection’s Sweet Tooth: How Glycans Mediate Infection and Disease Susceptibility

Blood Groups in Infection and Host Susceptibility

The VP8* Domain of Neonatal Rotavirus Strain G10P[11] Binds to Type II Precursor Glycans

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