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Corrigendum: Updated classification of norovirus genogroups and genotypes
ICTV Virus Taxonomy Profile: Caliciviridae
The family Caliciviridae includes viruses with single-stranded positive-sense RNA genomes of 7.4–8.3 kb. The most clinically important representatives are human noroviruses which are a leading cause of acute gastroenteritis in humans. Virions are non-enveloped with icosahedral symmetry. Members of seven genera infect mammals (Lagovirus Norovirus Nebovirus Recovirus Sapovirus Valovirus and Vesivirus) members of two genera infect birds (Bavovirus and Nacovirus) and members of two genera infect fish (Minovirus and Salovirus). This is a summary of the International Committee on Taxonomy of Viruses (ICTV) Report on the family Caliciviridae which is available at ictv.global/report/caliciviridae.
Updated classification of norovirus genogroups and genotypes
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 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 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.
Highly sensitive parechovirus CODEHOP PCR amplification of the complete VP1 gene for typing directly from clinical specimens and correct typing based on phylogenetic clustering
Purpose. Human parechoviruses (HPeVs) particularly type 3 can cause severe neurological disease and neonatal sepsis in infants. HPeV3 lacks the receptor-binding motif arginine-glycine aspartic acid (RGD) and is proposed to use a different receptor associated with severe disease. In contrast HPeV1 which contains the RGD motif is associated with mild disease. Rapid characterization of the presence/absence of this motif is essential for understanding their epidemiology and differential disease profiles. Current HPeV typing assays are based on partial capsid genes and often do not encompass the C-terminus where the RGD region is localized/absent. In addition these assays lack sensitivity to enable characterization within low viral-load samples such as cerebral spinal fluid.
Methodology. We developed a highly sensitive HPeV CODEHOP PCR which enables typing of parechoviruses directly from clinical samples while generating a complete VP1 gene including the C-terminus.
Results. The assay was HPeV-specific and has a sensitivity of 6.3 TCID50 ml−1 for HPeV1 and 0.63 TCID50 ml−1 for HPeV3. Analysis of the complete VP1 gene in comparison to partial VP1 fragments generated by previously published PCRs showed homologous clustering for most types. However phylogenetic analysis of partial VP1 fragments showed incongruent typing based on the 75 % homology classification rule. In particular the strains designated as type 17 were found to be either type 3 or 4 when using the (near-) complete VP1 fragment.
Conclusion. While enabling sensitive characterization of HPeVs directly from clinical samples the HPeV CODEHOP PCR enables the characterization of RGD and non-RGD strains and correct HPeV typing based on the complete VP1.
Comparison of norovirus genogroup I, II and IV seroprevalence among children in the Netherlands, 1963, 1983 and 2006
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.
Nucleotide sequence and expression of the spike (S) gene of canine coronavirus and comparison with the S proteins of feline and porcine coronaviruses
We have cloned sequenced and expressed the spike (S) gene of canine coronavirus (CCV; strain K378). Its deduced amino acid sequence has revealed features in common with other coronavirus S proteins: a stretch of hydrophobic amino acids at the amino terminus (the putative signal sequence) another hydrophobic region at the carboxy terminus (the membrane anchor) heptad repeats preceding the anchor and a cysteine-rich region located just downstream from it. Like other representatives of the same antigenic cluster (CCV-Insavc-1 strain feline infectious peritonitis and enteric corona- viruses porcine transmissible gastroenteritis and respiratory coronaviruses and the human coronavirus HCV 229E) the CCV S polypeptide lacks a proteolytic cleavage site present in many other coronavirus S proteins. Pairwise comparisons of the S amino acid sequences within the antigenic cluster demonstrated that the two CCV strains (K378 and Insavc-1) are 93·3% identical about as similar to each other as they are to the two feline coronaviruses. The porcine sequences are clearly more divergent mainly due to the large differences in the amino-terminal (residues 1 to 300) domains of the proteins; when only the carboxy-terminal parts (residues 301 and on) are considered the homologies between the canine feline and porcine S polypeptides are generally quite high with identities ranging from 90·8 % to 96·8 %. The human coronavirus is less related to the other members of the antigenic group. A phylogenetic tree constructed on the basis of the S sequences showed that the two CCVs are evolutionarily more related to the feline than to the porcine viruses. Expression of the CCV S gene using the vaccinia virus T7 RNA polymerase system yielded a protein of the expected M r (approximately 200K) which could be immunoprecipitated with an anti-feline infectious peritonitis virus polyclonal serum and which was indistinguishable from the S protein synthesized in CCV-infected cells.
The nucleotide sequence data presented in this paper have been submitted to the EMBL database and assigned the accession number X77047.
Mutation of Host Cell Determinants which Discriminate between Lytic and Persistent Mouse Hepatitis Virus Infection Results in a Fusion-resistant Phenotype
The expression of mouse hepatitis virus (MHV) E2-specific mRNA the E2 polypeptide and its associated cell fusing activity was monitored in various cell types inoculated with a recombinant vaccinia virus designated vMS containing the E2 gene. The results suggest that host cell permissiveness to MHV infection correlates with cellular susceptibility to membrane fusion mediated by the MHV E2 glycoprotein. In addition we utilized a genetic approach to the analysis of host cell functions involved in determining permissiveness to MHV. By using the chemical mutagen ethyl methanesulphonate mouse fibroblast cell mutants were generated and selected for their resistance to cell killing by MHV. When challenged with MHV all five mutants examined gave rise to persistent infections in contrast to wild-type L-2 cells which were rapidly killed by the virus. The results provide genetic evidence in support of a previous correlation proposed between MHV permissiveness and two host determinants namely susceptibility to MHV infection and to MHV-mediated cell fusion. Fusion resistance was specific to fusion mediated by the MHV E2 glycoprotein as shown in contact fusion assays between uninfected cells and cells infected either with MHV or with an E2-expressing recombinant vaccinia virus. In contrast mutant cells were not resistant to fusion after treatment with polyethylene glycol. The observed high rate of generation of these mutants suggests that the conversion of a fully MHV-susceptible cell to a semi-resistant one is a fairly common event possibly involving a single mutation. In this case resistance to MHV infection and to E2-mediated membrane fusion may depend on a common host function. This result provides prospects for the precise genetic and biochemical characterization of the steps involved in host cell permissiveness to MHV infection.