Editing Norovirus (section)

== Human genetics ==
Epidemiological studies have shown that individuals with different ABO(H) (histo-[[blood group]]) phenotypes are infected with NoV strains in a [[genotype]]-specific manner.<ref name="Infect"/><ref name="pmid20053852">{{cite journal |vauthors=Le Guyader FS, Krol J, Ambert-Balay K, Ruvoen-Clouet N, Desaubliaux B, Parnaudeau S, Le Saux JC, Ponge A, Pothier P, Atmar RL, Le Pendu J |title=Comprehensive analysis of a norovirus-associated gastroenteritis outbreak, from the environment to the consumer |journal=Journal of Clinical Microbiology |volume=48 |issue=3 |pages=915–920 |date=March 2010 |pmid=20053852 |pmc=2832421 |doi=10.1128/JCM.01664-09}}</ref> GII.4 includes global epidemic strains and binds to more histo-blood group antigens than other genogroups.<ref name="Infect" /> [[FUT2]] [[fucosyltransferase]] transfers a [[fucose]] sugar to the end of the [[blood group|ABO(H)]] precursor in [[gastrointestinal cell]]s and [[saliva gland]]s. The ABH-antigen produced is thought to act as a receptor for human norovirus: A non-functional [[fucosyltransferase]] FUT2 provides high protection from the most common norovirus strain, GII.4.<ref>{{cite journal |vauthors=Carlsson B, Kindberg E, Buesa J, Rydell GE, Lidón MF, Montava R, Abu Mallouh R, Grahn A, Rodríguez-Díaz J, Bellido J, Arnedo A, Larson G, Svensson L |title=The G428A nonsense mutation in FUT2 provides strong but not absolute protection against symptomatic GII.4 norovirus infection |journal=PLOS ONE |volume=4 |issue=5 |page=e5593 |date=May 2009 |pmid=19440360 |pmc=2680586 |doi=10.1371/journal.pone.0005593 |bibcode=2009PLoSO...4.5593C|doi-access=free }}</ref>

Homozygous carriers of any nonsense mutation in the FUT2 gene are called ''[[non-secretors]]'', as no ABH-antigen is produced. Approximately 20% of [[Caucasian race|Caucasians]] are non-secretors due to G428A and C571T nonsense mutations in FUT2 and therefore have strong&nbsp;– although not absolute&nbsp;– protection from the norovirus GII.4.<ref name=Rydell2011>{{cite journal |vauthors=Rydell GE, Kindberg E, Larson G, Svensson L |title=Susceptibility to winter vomiting disease: A sweet matter |journal=Rev. Med. Virol. |volume=21 |issue=6 |pages=370–382 |date=November 2011 |pmid=22025362 |doi=10.1002/rmv.704|s2cid=6679013 }}</ref> Non-secretors can still produce ABH antigens in erythrocytes, as the precursor is formed by FUT1.<ref name="Infect">{{cite journal |author=Shirato H |title=Norovirus and histo-blood group antigens |journal=Jpn. J. Infect. Dis. |volume=64 |issue=2 |pages=95–103 |year=2011 |doi=10.7883/yoken.64.95 |pmid=21519121|doi-access=free }}</ref> Some norovirus genotypes (GI.3) can infect non-secretors.<ref name=Nordgren2010>{{cite journal |vauthors=Nordgren J, Kindberg E, Lindgren PE, Matussek A, Svensson L |title=Norovirus gastroenteritis outbreak with a secretor-independent susceptibility pattern, Sweden |journal=Emerg. Infect. Dis. |volume=16 |issue=1 |pages=81–87 |date=January 2010 |pmid=20031047 |doi=10.3201/eid1601.090633 |pmc=2874438}}</ref>