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Conventional broad range RT-PCR and real time RT-PCR assays designed to detect human noroviruses (NoVs) also efficiently detect swine NoVs. Investigation of the primers and probe binding sites revealed strong homologies between swine NoVs genomic sequences and human primer sequences. These findings have a serious impact on food diagnostic methods and laboratories.

This study reports the molecular characterization of novel caliciviruses, the St-Valérien-like viruses, which were isolated from pig feces in the province of Quebec, Canada between 2005 and 2007. The genomes of St-Valérien-like viruses contain 6409 nucleotides and include two main open reading frames (ORFs). ORF1 encodes the non structural (NS) polyprotein and the major capsid protein (VP1) while ORF2 encodes the putative basic minor capsid protein. Typical conserved amino acid motifs predict a gene order reminiscent of calicivirus genomes. Phylogenetic, pairwise homology, and distance analyses performed on complete genomic sequences and partial amino acid sequences from the NTPase, polymerase, and major capsid protein segregated the St-Valérien-like viruses in a unique cluster sharing a common root with the Tulane virus and the noroviruses. Based on the genomic analyses presented, the St-Valérien-like viruses are members of a new genus of Caliciviridae for which we propose the name Valovirus.

Noroviruses and sapoviruses are members of the family Caliciviridae and emerging enteric pathogens of humans and animals. Since their discovery and characterization in swine, relatively few strains have been described in detail. In order to investigate their genetic diversity, a total of 266 fecal samples collected in the province of Quebec, Canada, between 2005 and 2007 were screened for the presence of caliciviruses by RT-PCR using broadly reactive primers. Genetically heterogeneous caliciviruses were detected on the majority of farms. Typical noroviruses related to known swine genotypes were present on 20% of the farms. Sapoviruses were detected on 75% of the farms and were the most heterogeneous group. Further characterization of selected strains in their 3' end parts was carried out for their classification and unveiled possibly new clusters of sapoviruses. No human-like noroviruses or sapoviruses were detected in the present study.

RNA silencing mediated by small RNAs (sRNAs) is a conserved regulatory process with key antiviral and antimicrobial roles in eukaryotes. A widespread counter-defensive strategy of viruses against RNA silencing is to deploy viral suppressors of RNA silencing (VSRs), epitomized by the P19 protein of tombusviruses, which sequesters sRNAs and compromises their downstream action. Here, we provide evidence that specific Nicotiana species are able to sense and, in turn, antagonize the effects of P19 by activating a highly potent immune response that protects tissues against Tomato bushy stunt virus infection. This immunity is salicylate- and ethylene-dependent, and occurs without microscopic cell death, providing an example of “extreme resistance” (ER). We show that the capacity of P19 to bind sRNA, which is mandatory for its VSR function, is also necessary to induce ER, and that effects downstream of P19-sRNA complex formation are the likely determinants of the induced resistance. Accordingly, VSRs unrelated to P19 that also bind sRNA compromise the onset of P19-elicited defense, but do not alter a resistance phenotype conferred by a viral protein without VSR activity. These results show that plants have evolved specific responses against the damages incurred by VSRs to the cellular silencing machinery, a likely necessary step in the never-ending molecular arms race opposing pathogens to their hosts., Author Summary Multiple and complex layers of defense help plants to combat pathogens. A first line of defense relies on the detection, via dedicated host-encoded receptors, of signature molecules (so called pathogen-associated molecular patterns, PAMPs) produced by pathogens. In turn, this PAMP-triggered immunity (PTI) may be itself antagonized by adapted pathogens that have evolved virulence effectors to target key PTI components. Host plants react to PTI suppression by producing disease resistance (R) proteins that recognize virulence effectors and activate highly specific resistance called Effector Triggered Immunity (ETI). It has been noted that RNA silencing, a sequence-specific antiviral defense response based on the production of virus-derived 21–24 nt small RNAs on the one hand, and its suppression by virulence effectors, called viral suppressors of RNA silencing (VSRs) on the other, are conceptually similar to PTI. Here we provide strong support to this hypothesis by showing that extreme resistance is indeed activated following detection, in specific host species, of the VSR activity of a viral virulence effector. The ensuing antiviral immunity displays many characteristics of ETI, suggesting that one or several R proteins must sense the integrity of the host silencing machinery.

At the request of the authors, PLOS Pathogens is retracting this publication following an investigation into concerns about the origin and assembly of Figure 6 and a mounting mistake in Figure 1B. The Northern blot depicted in Figure 6 contains several band duplications affecting the panels labelled 'IP@HA' and 'total RNA'. The figure was provided by Patrice Dunoyer during revision and was extracted from the Master thesis of a former student working under his supervision, without the prior consultation or consent of this student. The other authors of Sansregret et al. were not informed about the origin of this figure and, regrettably, its erroneous content escaped their attention both at the final revision and proofreading stages. During inspection of the original blots, we realised that the loading control of Figure 1B was not the correct one; we have found the cognate one and the loadings are comparable. Importantly, the cross-reacting band visible on Figure 1B also provides an internal loading control. This mistake was made by co-authors Raphael Sansregret and Kamal Bouarab. Further analysis of the raw material underlying the results depicted in Figure 6 was found to support the original conclusions drawn from it. The other conclusions of the published article also remain valid. However, given the nature and extent of data manipulation in Figure 6, the authors have collectively decided to retract the study. All authors concur with this statement and apologise for not having detected these errors. Kamal Bouarab and Olivier Voinnet, as the corresponding authors, take full responsibility for the publication of this erroneous paper and regret deeply the inconvenience caused.