Last data update: Jun 11, 2024. (Total: 46992 publications since 2009)
Records 1-10 (of 10 Records) |
Query Trace: Graaf C [original query] |
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Corrigendum: Updated classification of norovirus genogroups and genotypes.
Chhabra P , Graaf M , Parra GI , Chan MC , Green K , Martella V , Wang Q , White PA , Katayama K , Vennema H , Koopmans MPG , Vinjé J . J Gen Virol 2020 101 (8) 893 ![]() The genotypes referred to in this article were stated incorrectly. The genotype number 49 should have been stated as 48 and the number 27 should have been stated as 26. These errors occurred in the 'Abstract' section on page 1, in the ‘Discussion’ section on page 11, and within Fig. 5 on page 12. | | The sentence in the 'Abstract' should have read: | | ‘Using previously described 2× standard deviation (sd) criteria to group sequences into separate clusters, we expanded the number of genogroups to 10 (GI-GX) and the number of genotypes to 48 (9 GI, 26 GII, 3 GIII, 2 GIV, 2 GV, 2 GVI and 1 genotype each for GVII, GVIII, GIX [formerly GII.15] and GX).’ | | The sentence in the 'Discussion' section on page 11 should have read: | | ‘Viruses in these ten genogroups can be further divided into 48 confirmed capsid genotypes based on amino acids of the complete VP1 and 60 confirmed P-types based on partial nucleotide sequences of RdRp regions.’ | | Fig. 5 on page 12 erroneously stated ‘27+2T’. This should have been stated as ‘26+2T’. |
Detection of norovirus variant GII.4 Hong Kong in Asia and Europe, 2017-2019
Chan MC , Roy S , Bonifacio J , Zhang LY , Chhabra P , Chan JCM , Celma C , Igoy MA , Lau SL , Mohammad KN , Vinjé J , Vennema H , Breuer J , Koopmans M , de Graaf M . Emerg Infect Dis 2021 27 (1) 289-293 We report a new norovirus GII.4 variant, GII.4 Hong Kong, with low-level circulation in 4 Eurasia countries since mid-2017. Amino acid substitutions in key residues on the virus capsid associated with the emergence of pandemic noroviruses suggest that GII.4 Hong Kong has the potential to become the next pandemic variant. |
Updated classification of norovirus genogroups and genotypes.
Chhabra P , de Graaf M , Parra GI , Chan MC , Green K , Martella V , Wang Q , White PA , Katayama K , Vennema H , Koopmans MPG , Vinje J . J Gen Virol 2019 100 (10) 1393-1406 ![]() ![]() Noroviruses are genetically diverse RNA viruses associated with acute gastroenteritis in mammalian hosts. Phylogenetically, they can be segregated into different genogroups as well as P (polymerase)-groups and further into genotypes and P-types based on amino acid diversity of the complete VP1 gene and nucleotide diversity of the RNA-dependent RNA polymerase (RdRp) region of ORF1, respectively. In recent years, several new noroviruses have been reported that warrant an update of the existing classification scheme. Using previously described 2x standard deviation (sd) criteria to group sequences into separate clusters, we expanded the number of genogroups to 10 (GI-GX) and the number of genotypes to 49 (9 GI, 27 GII, 3 GIII, 2 GIV, 2 GV, 2 GVI and 1 genotype each for GVII, GVIII, GIX [formerly GII.15] and GX). Viruses for which currently only one sequence is available in public databases were classified into tentative new genogroups (GNA1 and GNA2) and genotypes (GII.NA1, GII.NA2 and GIV.NA1) with their definitive assignment awaiting additional related sequences. Based on nucleotide diversity in the RdRp region, noroviruses can be divided into 60 P-types (14 GI, 37 GII, 2 GIII, 1 GIV, 2 GV, 2 GVI, 1 GVII and 1 GX), 2 tentative P-groups and 14 tentative P-types. Future classification and nomenclature updates will be based on complete genome sequences and will be coordinated and disseminated by the international norovirus classification-working group. |
Global Spread of Norovirus GII.17 Kawasaki 308, 2014-2016
Chan MCW , Hu Y , Chen H , Podkolzin AT , Zaytseva EV , Komano J , Sakon N , Poovorawan Y , Vongpunsawad S , Thanusuwannasak T , Hewitt J , Croucher D , Collins N , Vinjé J , Pang XL , Lee BE , de Graaf M , van Beek J , Vennema H , Koopmans MPG , Niendorf S , Poljsak-Prijatelj M , Steyer A , White PA , Lun JH , Mans J , Hung TN , Kwok K , Cheung K , Lee N , Chan PKS . Emerg Infect Dis 2017 23 (8) 1359-1354 Analysis of complete capsid sequences of the emerging norovirus GII.17 Kawasaki 308 from 13 countries demonstrated that they originated from a single haplotype since the initial emergence in China in late 2014. Global spread of a sublineage SL2 was identified. A new sublineage SL3 emerged in China in 2016. |
CDC's Prevention Status Reports: Monitoring the status of public health policies and practices for improved performance and accountability
Young AC , Lowry G , Mumford K , Graaf C . J Public Health Manag Pract 2017 24 (2) 121-128 CONTEXT: Increasing the adoption and implementation of evidence-based policies and practices is a key strategy for improving public health. Although there is widespread agreement about the importance of implementing evidence-based public health policies and practices, there are gaps between what has been shown to be effective and what is implemented at the state level. OBJECTIVE: The Centers for Disease Control and Prevention (CDC) developed the Prevention Status Reports (PSRs), a performance measurement system, to highlight evidence-based public health policies and practices and catalyze state performance and quality improvement efforts across the nation. DESIGN: CDC selected a set of 10 topics representing some of the most important public health challenges in the nation. Stakeholders, including state health departments and other partners, helped conceptualize the PSRs and informed the development of the PSR framework, which provides an organizational structure for the system. CDC subject matter experts developed criteria for selecting policies and practices, indicators for each policy and practice, and a criteria-based rating system for each indicator. PARTICIPANTS AND SETTING: The PSRs were developed for all 50 states and the District of Columbia. MAIN OUTCOME: The PSRs were developed and serve as a performance measurement system for monitoring the adoption, reach, and implementation fidelity of evidence-based public health policies and practices nationwide. RESULTS: The PSRs include 33 policy and practice indicators across the 10 health topics. They use a simple 3-level rating system-green, yellow, and red-to report the extent to which each state (and the District of Columbia) has implemented the policy or practice in accordance with supporting evidence or expert recommendations. Results from aggregate analyses show positive change or improvement. CONCLUSION: The PSRs are a unique part of CDC's work to improve the performance and accountability of the public health system, serving as both a monitoring tool and a call to action to improve health outcomes. The PSRs can be used to track the reach of and fidelity to evidence-based policies and practices nationally over time, as well as inform state efforts to improve their use of evidence-based policies and practice. |
Comparison of norovirus genogroup I, II and IV seroprevalence among children in the Netherlands, 1963, 1983 and 2006.
van Beek J , de Graaf M , Xia M , Jiang X , Vinje J , Beersma M , de Bruin E , van de Vijver D , Holwerda M , van Houten M , Buisman AM , van Binnendijk R , Osterhaus AD , van der Klis F , Vennema H , Koopmans MP . J Gen Virol 2016 97 (9) 2255-64 ![]() Noroviruses are a major cause of acute gastroenteritis worldwide and are a genetically diverse group of viruses. Since 2002, an increasing number of norovirus outbreaks have been reported globally, but it is not clear whether this increase has been caused by a higher awareness or reflects the emergence of new genogroup II genotype 4 (GII.4) variants. The hypothesis that norovirus prevalence has increased post-2002 and is related to the emergence of GII.4 is tested in this study. Sera collected from children aged <5 years of three Dutch cross-sectional population based cohorts in 1963, 1983 and 2006/2007 (n=143, n=130 and n=376, respectively) were tested for specific serum IgG by protein array using antigens to GII.4 and a range of other antigens representing norovirus GI, GII and GIV genotypes. The protein array was validated by paired sera of norovirus infected patients and supernatants of B-cell cultures with single epitope specificity. Evidence for norovirus infection was found to be common among Dutch children in each cohort, but the prevalence towards different genotypes changed over time. At the genogroup level, GI seroprevalence decreased significantly between 1963 and 2006/2007, while a significant increase of GII and, in particular, specific antibodies of the genotype GII.4 was detected in the 2006/2007 cohort. There were no children with only GII.4 antibodies in the 1963 cohort. This study shows that the high GII.4 norovirus incidence in very young children is a recent phenomenon. These findings are of importance for vaccine development and trials that are currently focusing mostly on GII.4 viruses. |
Comparative genomics of Campylobacter fetus from reptiles and mammals reveals divergent evolution in host-associated lineages.
Gilbert MJ , Miller WG , Yee E , Zomer AL , van der Graaf-van Bloois L , Fitzgerald C , Forbes KJ , Meric G , Sheppard SK , Wagenaar JA , Duim B . Genome Biol Evol 2016 8 (6) 2006-19 ![]() Campylobacter fetus currently comprises three recognized subspecies, which display distinct host association. C fetus subsp. fetus and C fetus subsp. venerealis are both associated with endothermic mammals, primarily ruminants, whereas C fetus subsp. testudinum is primarily associated with ectothermic reptiles. Both C. fetus subsp. testudinum and C. fetus subsp. fetus have been associated with severe infections, often with a systemic component, in immunocompromised humans. To study the genetic factors associated with the distinct host dichotomy in C. fetus, whole-genome sequencing and comparison of mammal- and reptile-associated C fetus was performed. The genomes of C fetus subsp. testudinum isolated from either reptiles or humans were compared to elucidate the genetic factors associated with pathogenicity in humans. Genomic comparisons showed conservation of gene content and organization amongst C fetus subspecies, but a clear distinction between mammal- and reptile-associated C fetus was observed. Several genomic regions appeared to be subspecies specific, including a putative tricarballylate catabolism pathway, exclusively present in C fetus subsp. testudinum strains. Within C fetus subsp. testudinum, sapA, sapB, and sapAB type strains were observed. The recombinant locus iamABC (mlaFED) was exclusively associated with invasive C fetus subsp. testudinum strains isolated from humans. A phylogenetic reconstruction was consistent with divergent evolution in host-associated strains and the existence of a barrier to lateral gene transfer between mammal- and reptile-associated C fetus Overall, this study shows that reptile-associated C fetus subsp. testudinum is genetically divergent from mammal-associated C fetus subspecies. |
Emergence of a novel GII.17 norovirus – End of the GII.4 era?
de Graaf M , van Beek J , Vennema H , Podkolzin AT , Hewitt J , Bucardo F , Templeton K , Mans J , Nordgren J , Reuter G , Lynch M , Rasmussen LD , Iritani N , Chan MC , Martella V , Ambert-Balay K , Vinjé J , White PA , Koopmans MP . Euro Surveill 2015 20 (26) In the winter of 2014/15 a novel GII.P17-GII.17 norovirus strain (GII.17 Kawasaki 2014) emerged, as a major cause of gastroenteritis outbreaks in China and Japan. Since their emergence these novel GII.P17-GII.17 viruses have replaced the previously dominant GII.4 genotype Sydney 2012 variant in some areas in Asia but were only detected in a limited number of cases on other continents. This perspective provides an overview of the available information on GII.17 viruses in order to gain insight in the viral and host characteristics of this norovirus genotype. We further discuss the emergence of this novel GII.P17-GII.17 norovirus in context of current knowledge on the epidemiology of noroviruses. It remains to be seen if the currently dominant norovirus strain GII.4 Sydney 2012 will be replaced in other parts of the world. Nevertheless, the public health community and surveillance systems need to be prepared in case of a potential increase of norovirus activity in the next seasons caused by this novel GII.P17-GII.17 norovirus. |
Human norovirus culture in B cells
Jones MK , Grau KR , Costantini V , Kolawole AO , de Graaf M , Freiden P , Graves CL , Koopmans M , Wallet SM , Tibbetts SA , Schultz-Cherry S , Wobus CE , Vinje J , Karst SM . Nat Protoc 2015 10 (12) 1939-47 Human noroviruses (HuNoVs) are a leading cause of foodborne disease and severe childhood diarrhea, and they cause a majority of the gastroenteritis outbreaks worldwide. However, the development of effective and long-lasting HuNoV vaccines and therapeutics has been greatly hindered by their uncultivability. We recently demonstrated that a HuNoV replicates in human B cells, and that commensal bacteria serve as a cofactor for this infection. In this protocol, we provide detailed methods for culturing the GII.4-Sydney HuNoV strain directly in human B cells, and in a coculture system in which the virus must cross a confluent epithelial barrier to access underlying B cells. We also describe methods for bacterial stimulation of HuNoV B cell infection and for measuring viral attachment to the surface of B cells. Finally, we highlight variables that contribute to the efficiency of viral replication in this system. Infection assays require 3 d and attachment assays require 3 h. Analysis of infection or attachment samples, including RNA extraction and RT-qPCR, requires approximately 6 h. |
Antigenic and genetic characteristics of swine-origin 2009 A(H1N1) influenza viruses circulating in humans
Garten RJ , Davis CT , Russell CA , Shu B , Lindstrom S , Balish A , Sessions WM , Xu X , Skepner E , Deyde V , Okomo-Adhiambo M , Gubareva L , Barnes J , Smith CB , Emery SL , Hillman MJ , Rivailler P , Smagala J , de Graaf M , Burke DF , Fouchier RA , Pappas C , Alpuche-Aranda CM , Lopez-Gatell H , Olivera H , Lopez I , Myers CA , Faix D , Blair PJ , Yu C , Keene KM , Dotson PD Jr , Boxrud D , Sambol AR , Abid SH , St George K , Bannerman T , Moore AL , Stringer DJ , Blevins P , Demmler-Harrison GJ , Ginsberg M , Kriner P , Waterman S , Smole S , Guevara HF , Belongia EA , Clark PA , Beatrice ST , Donis R , Katz J , Finelli L , Bridges CB , Shaw M , Jernigan DB , Uyeki TM , Smith DJ , Klimov AI , Cox NJ . Science 2009 325 (5937) 197-201 ![]() Since its identification in April 2009, an A(H1N1) virus containing a unique combination of gene segments from both North American and Eurasian swine lineages has continued to circulate in humans. The lack of similarity between the 2009 A(H1N1) virus and its nearest relatives indicates that its gene segments have been circulating undetected for an extended period. Its low genetic diversity suggests that the introduction into humans was a single event or multiple events of similar viruses. Molecular markers predictive of adaptation to humans are not currently present in 2009 A(H1N1) viruses, suggesting that previously unrecognized molecular determinants could be responsible for the transmission among humans. Antigenically the viruses are homogeneous and similar to North American swine A(H1N1) viruses but distinct from seasonal human A(H1N1). |
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