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Open AccessArticle

Bile Facilitates Human Norovirus Interactions with Diverse Histoblood Group Antigens, Compensating for Capsid Microvariation Observed in 2016–2017 GII.2 Strains

Department of Epidemiology, University of North Carolina, Chapel Hill, NC 27599, USA
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Viruses 2020, 12(9), 989; https://doi.org/10.3390/v12090989
Received: 3 August 2020 / Revised: 1 September 2020 / Accepted: 1 September 2020 / Published: 5 September 2020
(This article belongs to the Section Animal Viruses)
Human norovirus (HuNoV) is the leading cause of global infectious acute gastroenteritis, causing ~20% of reported diarrheal episodes. Typically, GII.4 strains cause 50–70% of yearly outbreaks, and pandemic waves of disease approximately every 2–7 years due to rapid evolution. Importantly, GII.4 dominance is occasionally challenged by the sudden emergence of other GII strains, most recently by GII.2 strains which peaked in 2016–2017, dramatically increasing from 1% to 20% of total HuNoV outbreaks. To determine if viral capsid evolution may account for the sudden rise in GII.2 outbreaks, Virus Like Particles (VLPs) of two 2016–2017 GII.2 strains were compared by antigenic and histo blood group antigen (HBGA) binding profiles to the prototypic 1976 GII.2 Snow Mountain Virus (SMV) strain. Despite >50 years of GII.2 strain persistence in human populations, limited sequence diversity and antigenic differences were identified between strains. However, capsid microvariation did affect HBGA binding patterns, with contemporary strains demonstrating decreased avidity for type A saliva. Furthermore, bile salts increased GII.2 VLP avidity for HBGAs, but did not alter antigenicity. These data indicate that large changes in antigenicity or receptor binding are unlikely to explain GII.2 emergence, in contrast to the pandemic GII.4 strains, and indicate that host factors such as waning or remodeling of serum or mucosal immunity likely contributed to the surge in GII.2 prevalence. View Full-Text
Keywords: norovirus; immunity; bile; blockade antibody; histo blood group antigen norovirus; immunity; bile; blockade antibody; histo blood group antigen
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MDPI and ACS Style

Mallory, M.L.; Lindesmith, L.C.; Brewer-Jensen, P.D.; Graham, R.L.; Baric, R.S. Bile Facilitates Human Norovirus Interactions with Diverse Histoblood Group Antigens, Compensating for Capsid Microvariation Observed in 2016–2017 GII.2 Strains. Viruses 2020, 12, 989. https://doi.org/10.3390/v12090989

AMA Style

Mallory ML, Lindesmith LC, Brewer-Jensen PD, Graham RL, Baric RS. Bile Facilitates Human Norovirus Interactions with Diverse Histoblood Group Antigens, Compensating for Capsid Microvariation Observed in 2016–2017 GII.2 Strains. Viruses. 2020; 12(9):989. https://doi.org/10.3390/v12090989

Chicago/Turabian Style

Mallory, Michael L.; Lindesmith, Lisa C.; Brewer-Jensen, Paul D.; Graham, Rachel L.; Baric, Ralph S. 2020. "Bile Facilitates Human Norovirus Interactions with Diverse Histoblood Group Antigens, Compensating for Capsid Microvariation Observed in 2016–2017 GII.2 Strains" Viruses 12, no. 9: 989. https://doi.org/10.3390/v12090989

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