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      Mendelian resistance to human norovirus infections

      review-article
      a , * , a , b , c , d , c
      Seminars in Immunology
      Published by Elsevier Ltd.
      CCR5, chemokine receptor 5, Fuc, fucose, FUT2, α1,2fucosyltransferase, Gal, galactose, GG, genogroup, Glc, glucose, HBGA, histo-blood group antigen, HIV, human immunodeficiency virus, IgG, immunoglobulin G, Le, Lewis antigen, NAc, N-acetyl, NV, Norwalk virus, NTPase, nucleoside triphosphate, ORF, open reading frame, Pol, polymerase, Pro, proteinase, RHDV, Rabbit Hemorrhagic Disease Virus, RNA, ribonucleic acid, RT-PCR, reverse transcriptase polymerase chain reaction, SMV, Snow Mountain virus, VLP, virus-like particles, VP, virus protein, Norovirus, FUT2, Secretor, Histo-blood group antigen, Gastroenteritis

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          Abstract

          Noroviruses have emerged as a major cause of acute gastroenteritis in humans of all ages. Despite high infectivity of the virus and lack of long-term immunity, volunteer and authentic studies has suggested the existence of inherited protective factors. Recent studies have shown that histo-blood group antigens (HBGAs) and in particular secretor status controlled by the α1,2fucosyltransferase FUT2 gene determine susceptibility to norovirus infections, with nonsecretors (FUT2−/−), representing 20% of Europeans, being highly resistant to symptomatic infections with major strains of norovirus. Moreover, the capsid protein from distinct strains shows different HBGA specificities, suggesting a host–pathogen co-evolution driven by carbohydrate–protein interactions.

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          Most cited references83

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          Biological and biomedical implications of the co-evolution of pathogens and their hosts.

          Co-evolution between host and pathogen is, in principle, a powerful determinant of the biology and genetics of infection and disease. Yet co-evolution has proven difficult to demonstrate rigorously in practice, and co-evolutionary thinking is only just beginning to inform medical or veterinary research in any meaningful way, even though it can have a major influence on how genetic variation in biomedically important traits is interpreted. Improving our understanding of the biomedical significance of co-evolution will require changing the way in which we look for it, complementing the phenomenological approach traditionally favored by evolutionary biologists with the exploitation of the extensive data becoming available on the molecular biology and molecular genetics of host-pathogen interactions.
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            CCR5 deficiency increases risk of symptomatic West Nile virus infection

            West Nile virus (WNV) is a reemerging pathogen that causes fatal encephalitis in several species, including mouse and human. Recently, we showed that the chemokine receptor CCR5 is critical for survival of mice infected with WNV, acting at the level of leukocyte trafficking to the brain. To test whether this receptor is also protective in man, we determined the frequency of CCR5Δ32, a defective CCR5 allele found predominantly in Caucasians, in two independent cohorts of patients, one from Arizona and the other from Colorado, who had laboratory-confirmed, symptomatic WNV infection. The distribution of CCR5Δ32 in a control population of healthy United States Caucasian random blood donors was in Hardy-Weinberg equilibrium and CCR5Δ32 homozygotes represented 1.0% of the total group (n = 1,318). In contrast, CCR5Δ32 homozygotes represented 4.2% of Caucasians in the Arizona cohort (odds ratios [OR] = 4.4 [95% confidence interval [CI], 1.6–11.8], P = 0.0013) and 8.3% of Caucasians in the Colorado cohort (OR = 9.1 [95% CI, 3.4–24.8], P < 0.0001). CCR5Δ32 homozygosity was significantly associated with fatal outcome in the Arizona cohort (OR = 13.2 [95% CI, 1.9–89.9], P = 0.03). We conclude that CCR5 mediates resistance to symptomatic WNV infection. Because CCR5 is also the major HIV coreceptor, these findings have important implications for the safety of CCR5-blocking agents under development for HIV/AIDS.
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              Human milk oligosaccharides are associated with protection against diarrhea in breast-fed infants.

              To determine the association between maternal milk levels of 2-linked fucosylated oligosaccharide and prevention of diarrhea as a result of Campylobacter, caliciviruses, and diarrhea of all causes in breast-fed infants. Data and banked samples were analyzed from 93 breast-feeding mother-infant pairs who were prospectively studied during 1988-1991 from birth to 2 years with infant feeding and diarrhea data collected weekly; diarrhea was diagnosed by a study physician. Milk samples obtained 1 to 5 weeks postpartum were analyzed for oligosaccharide content. Data were analyzed by Poisson regression. Total 2-linked fucosyloligosaccharide in maternal milk ranged from 0.8 to 20.8 mmol/L (50%-92% of milk oligosaccharide). Moderate-to-severe diarrhea of all causes (n=77 cases) occurred less often (P=.001) in infants whose milk contained high levels of total 2-linked fucosyloligosaccharide as a percent of milk oligosaccharide. Campylobacter diarrhea (n=31 cases) occurred less often (P=.004) in infants whose mother's milk contained high levels of 2'-FL, a specific 2-linked fucosyloligosaccharide, and calicivirus diarrhea (n=16 cases) occurred less often (P=.012) in infants whose mother's milk contained high levels of lacto-N-difucohexaose (LDFH-I), another 2-linked fucosyloligosaccharide. This study provides novel evidence suggesting that human milk oligosaccharides are clinically relevant to protection against infant diarrhea.
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                Author and article information

                Contributors
                Journal
                Semin Immunol
                Semin. Immunol
                Seminars in Immunology
                Published by Elsevier Ltd.
                1044-5323
                1096-3618
                14 September 2006
                December 2006
                14 September 2006
                : 18
                : 6
                : 375-386
                Affiliations
                [a ]Inserm U601, University of Nantes, Institute of Biology, 9 Quai Moncousu, 44093 Nantes, Cedex 01, France
                [b ]National Veterinary School of Nantes, Route de Gachet, BP 40706 Nantes, Cedex 03, France
                [c ]Division of Molecular Virology, University of Linköping, Sweden
                [d ]Department of Forensic Genetics, National Board of Forensic Medicine, Linköping, Sweden
                Author notes
                [* ]Corresponding author. Tel.: +33 240 08 40 99; fax: +33 240 08 40 82. jlependu@ 123456nantes.inserm.fr
                Article
                S1044-5323(06)00103-5
                10.1016/j.smim.2006.07.009
                7129677
                16973373
                3f25668d-c9ef-4023-b628-90b5338f4051
                Copyright © 2006 Published by Elsevier Ltd.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

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                Categories
                Article

                Immunology
                ccr5, chemokine receptor 5,fuc, fucose,fut2, α1,2fucosyltransferase,gal, galactose,gg, genogroup,glc, glucose,hbga, histo-blood group antigen,hiv, human immunodeficiency virus,igg, immunoglobulin g,le, lewis antigen,nac, n-acetyl,nv, norwalk virus,ntpase, nucleoside triphosphate,orf, open reading frame,pol, polymerase,pro, proteinase,rhdv, rabbit hemorrhagic disease virus,rna, ribonucleic acid,rt-pcr, reverse transcriptase polymerase chain reaction,smv, snow mountain virus,vlp, virus-like particles,vp, virus protein,norovirus,fut2,secretor,histo-blood group antigen,gastroenteritis

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