The Norovirus Epidemiologic Triad: Predictors of Severe Outcomes in US Norovirus Outbreaks, 2009–2016

Burke, Rachel M; Shah, Minesh; Wikswo, Mary E.; Barclay, Leslie; Kambhampati, Anita; Marsh, Zachary; Cannon, Jennifer L.; Parashar, Umesh D.; Vinjé, Jan; Hall, Aron J.

doi:10.1093/infdis/jiy569

Cited by 60 publications

(55 citation statements)

References 30 publications

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“…This discrepancy might be related to different outbreak settings. A recently published study suggested that GII.4 NoV outbreaks were significantly more likely to be associated with foodborne transmission in non-healthcare settings [ 13 ]. Our results showed that GII.4 Sydney outbreaks were more likely to occur in colleges/universities, while prior studies reported a higher proportion of healthcare-associated outbreaks [ 4 , 14 ].…”

Section: Resultsmentioning

confidence: 99%

Epidemiologic characteristics of outbreaks of three norovirus genotypes (GII.2, GII.17 and GII.4 Sydney) in Guangzhou, China, from 2012 to 2018

Wang

Chen

et al. 2019

Epidemiol. Infect.

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To compare the epidemiologic features (e.g. settings and transmission mode) and patient clinical characteristics associated with outbreaks of different norovirus (Nov) strains, we retrospectively analysed data of Nov outbreaks occurring in Guangzhou, China from 2012 to 2018. The results suggested that outbreaks of Nov GII.2, GII.17 and GII.4 Sydney exhibited different outbreak settings, transmission modes and symptoms. GII.2 outbreaks mainly occurred in kindergartens, elementary and high schools and were transmitted mainly through person-to-person contact. By contrast, GII.4 Sydney outbreaks frequently occurred in colleges and were primarily associated with foodborne transmission. Cases from GII.2 and GII.17 outbreaks reported vomiting more frequently than those from outbreaks associated with GII.4 Sydney.

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Section: Resultsmentioning

confidence: 99%

Epidemiologic characteristics of outbreaks of three norovirus genotypes (GII.2, GII.17 and GII.4 Sydney) in Guangzhou, China, from 2012 to 2018

Wang

Chen

et al. 2019

Epidemiol. Infect.

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“…from the National Outbreak Reporting System, yielding comprehensive surveillance in the United States that enables multifactorial characterization of norovirus outbreaks (9).…”

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confidence: 99%

Norovirus Outbreak Surveillance, China, 2016–2018

Jin¹,

Wu²,

Kong³

et al. 2020

Emerg. Infect. Dis.

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H uman noroviruses are the leading cause of outbreaks of acute gastroenteritis, associated with ≈50% of all outbreaks worldwide (1). Norovirus outbreaks are frequently reported in semiclosed institutions, such as hospitals, nursing homes, schools, and childcare centers (2). The virus is primarily transmitted directly from person to person or indirectly through contaminated surfaces, food, or water (1). The relative stability of noroviruses on environmental surfaces makes infection control challenging (3). Several candidate norovirus vaccines are in clinical trials (4). Noroviruses are single-stranded RNA viruses that belong to the genus Norovirus, family Caliciviridae. The genome is organized into 3 open reading frames (ORFs): ORF1 encodes polyprotein, ORF2 encodes the major capsid protein (VP1), and ORF3 encodes the minor (VP2) capsid protein. The viruses are classified into at least 7 genogroups (G), of which viruses from GI, GII, and GIV infect humans (5,6). On the basis of the diversity of VP1, these genogroups can be further divided into at least 33 genotypes: 9 GI, 22 GII, and 2 GIV (7). In addition, on the basis of the diversity of the polymerase region of ORF1, >14 GI polymerase (GI.P) types and 27 GII.P types have been described (7). Because of the frequent recombination at the ORF1/ORF2 junction region, a dual-typing system has been proposed for GI and GII noroviruses (7). Since 2002, genogroup II, genotype 4 (GII.4), noroviruses have been associated with most norovirus outbreaks globally, and new GII.4 variants have emerged every 2-3 years (8). Monitoring the trends in the distribution of the various genotypes and possible association of certain strains with a more severe disease outcome is important for understanding and controlling norovirus epidemics (9). Several norovirus outbreak surveillance networks, including NoroNet (10) and CaliciNet (7,11), have been developed during the past decade. NoroNet captures molecular and epidemiologic data on norovirus outbreaks and sporadic cases submitted by 19 participating countries across Europe and Asia and by Australia. CaliciNet is a norovirus outbreak surveillance network in the United States in which state and local public health laboratories electronically submit laboratory data, including sequences from norovirus outbreaks, to a central database (https://www. cdc.gov/norovirus/reporting/calicinet/data.html). CaliciNet data are integrated with epidemiologic data

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“…Mechanisms of emergence of GII.2 human noroviruses are not as clearly understood as those of GII.4 pandemic strains, which have been characterized by antigenic drift in known antibody epitopes and recombination events with polymerases from other human norovirus genotypes [17,19,21,[27][28][29][30]. Current methodology centers around analyzing antigenic variation of capsids due to the lack of targeted assays to evaluate the effect of variation within polymerase and VP2 sequences.…”

Section: Discussionmentioning

confidence: 99%

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

Mallory

Lindesmith

Brewer-Jensen

et al. 2020

Viruses

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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.

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The Norovirus Epidemiologic Triad: Predictors of Severe Outcomes in US Norovirus Outbreaks, 2009–2016

Cited by 60 publications

References 30 publications

Epidemiologic characteristics of outbreaks of three norovirus genotypes (GII.2, GII.17 and GII.4 Sydney) in Guangzhou, China, from 2012 to 2018

Epidemiologic characteristics of outbreaks of three norovirus genotypes (GII.2, GII.17 and GII.4 Sydney) in Guangzhou, China, from 2012 to 2018

Norovirus Outbreak Surveillance, China, 2016–2018

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

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