Susceptibility to winter vomiting disease: a sweet matter
SUMMARY Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200 000 deaths each year in developing countries. Although the virus is highly contagious, volunteer...
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Published in | Reviews in medical virology Vol. 21; no. 6; pp. 370 - 382 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Chichester, UK
John Wiley & Sons, Ltd
01.11.2011
Wiley Periodicals Inc |
Subjects | |
Online Access | Get full text |
ISSN | 1052-9276 1099-1654 1099-1654 |
DOI | 10.1002/rmv.704 |
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Abstract | SUMMARY
Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200 000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene (FUT2) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo‐blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease. Copyright © 2011 John Wiley & Sons, Ltd. |
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AbstractList | SUMMARY Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene (FUT2) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo-blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease. Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200,000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene (FUT2) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo-blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease.Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200,000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene (FUT2) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo-blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease. SUMMARY Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200 000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene (FUT2) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo‐blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease. Copyright © 2011 John Wiley & Sons, Ltd. Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200,000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene (FUT2) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo-blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease. Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200 000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene ( FUT2 ) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo‐blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease. Copyright © 2011 John Wiley & Sons, Ltd. SUMMARY Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause >200000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene (FUT2) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo-blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease. Copyright © 2011 John Wiley & Sons, Ltd. Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus has been estimated to cause andgt;200 000 deaths each year in developing countries. Although the virus is highly contagious, volunteer and field studies have shown that a subset of individuals appears resistant to infections. A single nucleotide mutation (G428A) in the fucosyltransferase gene (FUT2) on chromosome 19 provides strong protection from infection in 20% of the white population. Histo-blood group ABO(H) antigens with terminal fucose are believed to function as receptors for human norovirus in the gastrointestinal tract, but also negatively charged potential receptors have been identified. Norovirus infection is a unique example where a single nucleotide mutation in a fucosyltransferase gene plays a crucial role in susceptibility to one of the most common viral diseases. This review discusses the role of host genetics and carbohydrate structures in susceptibility to winter vomiting disease. |
Author | Svensson, Lennart Larson, Göran Kindberg, Elin Rydell, Gustaf E. |
Author_xml | – sequence: 1 givenname: Gustaf E. surname: Rydell fullname: Rydell, Gustaf E. organization: Dept. of Clinical Chemistry and Transfusion Medicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden – sequence: 2 givenname: Elin surname: Kindberg fullname: Kindberg, Elin organization: Div. of Molecular Virology, Medical Faculty, University of Linköping, Linköping, Sweden – sequence: 3 givenname: Göran surname: Larson fullname: Larson, Göran organization: Dept. of Clinical Chemistry and Transfusion Medicine, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden – sequence: 4 givenname: Lennart surname: Svensson fullname: Svensson, Lennart email: lennart.t.svensson@liu.se, L. Svensson, Molecular Virology, Clinical and Experimental medicine, University of Linköping, Sweden., lennart.t.svensson@liu.se organization: Div. of Molecular Virology, Medical Faculty, University of Linköping, Linköping, Sweden |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22025362$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-72820$$DView record from Swedish Publication Index https://gup.ub.gu.se/publication/150133$$DView record from Swedish Publication Index |
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From structural to functional glycomics: core substitutions as molecular switches for shape and lectin affinity 2010; 12 1994; 330 2010; 16 2005; 253 2009; 81 1994; 170 2009; 83 1999; 286 2008; 5 2008; 105 1971; 123 2008; 225 1980; 92 1996; 70 2005; 24 2004; 30 2009; 58 2010; 24 1991; 88 2002; 185 2009; 90 1993; 31 2004; 78 2003; 9 2007; 450 2010; 155 2009; 200 1972; 10 1999; 179 2000; 287 2005; 37 2010; 2 2009; 19 2008; 198 2008; 197 2005; 77 2005; 79 1977; 297 2006; 124 2005; 191 1973; 288 2004; 85 2005; 192 2010; 76 2009; 24 2004; 42 1973; 79 2002; 76 2008; 14 2005; 40 2006; 19 2005; 43 1974; 129 1993 2006; 194 1995; 2 1996; 13 2004; 305 2007; 13 1995; 270 2009; 26 2010; 84 2003; 77 1990; 161 1984; 170 2001; 83 2006; 80 2004; 53 1987; 138 2009; 390 2006; 44 2000; 74 2002; 122 2000; 108 2004; 56 1975; 68 1993; 195 2008; 46 2007; 81 1982; 115 2008; 379 2009; 5 2009; 4 2009; 384 2008; 178 2006; 346 1992; 66 2007; 45 2008; 82 2005; 11 2003; 188 2008; 80 e_1_2_16_23_1 e_1_2_16_46_1 e_1_2_16_27_1 e_1_2_16_117_1 e_1_2_16_42_1 e_1_2_16_88_1 e_1_2_16_65_1 e_1_2_16_113_1 e_1_2_16_84_1 e_1_2_16_61_1 e_1_2_16_80_1 e_1_2_16_101_1 e_1_2_16_15_1 e_1_2_16_38_1 e_1_2_16_19_1 e_1_2_16_34_1 e_1_2_16_57_1 e_1_2_16_30_1 e_1_2_16_53_1 e_1_2_16_76_1 e_1_2_16_99_1 e_1_2_16_105_1 e_1_2_16_11_1 e_1_2_16_109_1 e_1_2_16_95_1 e_1_2_16_72_1 e_1_2_16_91_1 e_1_2_16_9_1 e_1_2_16_112_1 e_1_2_16_5_1 e_1_2_16_26_1 e_1_2_16_49_1 e_1_2_16_45_1 e_1_2_16_68_1 e_1_2_16_41_1 e_1_2_16_64_1 e_1_2_16_87_1 e_1_2_16_22_1 e_1_2_16_60_1 e_1_2_16_83_1 e_1_2_16_114_1 Mollison PL (e_1_2_16_56_1) 1993 e_1_2_16_14_1 e_1_2_16_18_1 e_1_2_16_37_1 e_1_2_16_79_1 e_1_2_16_98_1 e_1_2_16_52_1 e_1_2_16_33_1 e_1_2_16_75_1 e_1_2_16_102_1 e_1_2_16_71_1 e_1_2_16_94_1 e_1_2_16_10_1 e_1_2_16_106_1 e_1_2_16_8_1 e_1_2_16_90_1 e_1_2_16_25_1 e_1_2_16_29_1 e_1_2_16_67_1 e_1_2_16_48_1 e_1_2_16_63_1 e_1_2_16_44_1 e_1_2_16_86_1 e_1_2_16_21_1 e_1_2_16_115_1 e_1_2_16_40_1 e_1_2_16_82_1 Jiang X (e_1_2_16_20_1) 1992; 66 Kapikian AZ (e_1_2_16_4_1) 1972; 10 Green KY (e_1_2_16_69_1) 1993; 31 e_1_2_16_13_1 e_1_2_16_17_1 e_1_2_16_36_1 e_1_2_16_59_1 e_1_2_16_78_1 e_1_2_16_32_1 e_1_2_16_55_1 e_1_2_16_74_1 e_1_2_16_103_1 e_1_2_16_97_1 e_1_2_16_70_1 e_1_2_16_51_1 e_1_2_16_107_1 e_1_2_16_93_1 e_1_2_16_7_1 e_1_2_16_110_1 e_1_2_16_3_1 e_1_2_16_24_1 e_1_2_16_28_1 e_1_2_16_47_1 e_1_2_16_89_1 e_1_2_16_2_1 e_1_2_16_43_1 e_1_2_16_66_1 e_1_2_16_85_1 e_1_2_16_62_1 e_1_2_16_81_1 e_1_2_16_116_1 e_1_2_16_100_1 e_1_2_16_39_1 e_1_2_16_12_1 e_1_2_16_35_1 e_1_2_16_16_1 e_1_2_16_58_1 e_1_2_16_31_1 e_1_2_16_77_1 e_1_2_16_104_1 e_1_2_16_96_1 e_1_2_16_54_1 e_1_2_16_73_1 e_1_2_16_108_1 e_1_2_16_92_1 e_1_2_16_50_1 e_1_2_16_111_1 e_1_2_16_6_1 |
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Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide.... Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide. The virus... SUMMARY Norovirus, the cause of winter vomiting disease, has emerged in recent years to be a major cause of sporadic and epidemic gastroenteritis worldwide.... |
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SubjectTerms | Annan klinisk medicin Blood Group Antigens - chemistry Blood Group Antigens - metabolism Caliciviridae Infections - epidemiology Caliciviridae Infections - genetics Caliciviridae Infections - virology Carbohydrates chromosome 19 Developing countries Epidemics fucose Fucosyltransferases - genetics Galactoside 2-alpha-L-fucosyltransferase Gastroenteritis Gastroenteritis - epidemiology Gastroenteritis - genetics Gastroenteritis - virology Gastrointestinal tract Genetic Predisposition to Disease Humans Infection Medical Biotechnology (Focus on Cell Biology (incl. Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy) MEDICIN MEDICINE Medicinsk bioteknologi (Inriktn. mot cellbiologi (inkl. stamcellsbiologi), molekylärbiologi, mikrobiologi, biokemi eller biofarmaci) Microbiology in the Medical Area Mikrobiologi inom det medicinska området Mutation Norovirus Norovirus - pathogenicity Nucleotides Other Clinical Medicine Polymorphism, Single Nucleotide Receptor mechanisms Receptors, Virus - chemistry Receptors, Virus - metabolism Seasons Sweet taste Vomiting Vomiting - epidemiology Vomiting - etiology Vomiting - virology |
Title | Susceptibility to winter vomiting disease: a sweet matter |
URI | https://api.istex.fr/ark:/67375/WNG-8Q6DSNR7-7/fulltext.pdf https://onlinelibrary.wiley.com/doi/abs/10.1002%2Frmv.704 https://www.ncbi.nlm.nih.gov/pubmed/22025362 https://www.proquest.com/docview/1766842768 https://www.proquest.com/docview/1017972742 https://www.proquest.com/docview/900642431 https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-72820 https://gup.ub.gu.se/publication/150133 |
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