Post-entry blockade of small ruminant lentiviruses by wild ruminants

Sanjosé, Leticia; Crespo, Helena; Blatti-Cardinaux, Laure Sarah Pauline; Glaria, Idoia; Martínez‐Carrasco, Carlos; Berriatua, E.; Amorena, B.; Andrés, D. de; Bertoni, Giuseppe; Reina, Ramsés

doi:10.1186/s13567-015-0288-7

Cited by 58 publications

(96 citation statements)

References 68 publications

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“…Compared to strain Ep-1PNA367, most of the nucleoli of strain Ep-1PNA367T1 were disintegrated with dispersed chromatin, and some mitochondria were destroyed or swelled (Fig 1C). More interestingly, some spherical virus-like particles (VLPs) with sizes of 65~70 nm in diameter were localized near the nuclear membrane area (Fig 1C), which is reminiscent of viral factory-like areas encapsulated with double membrane structure, as previously reported in virus-infected plants [50]. Similar structures were not observed in strain Ep-1PNA367.…”

Section: Resultssupporting

confidence: 79%

Virus-mediated suppression of host non-self recognition facilitates horizontal transmission of heterologous viruses

Chéng

Fù

et al. 2017

PLoS Pathog

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Non-self recognition is a common phenomenon among organisms; it often leads to innate immunity to prevent the invasion of parasites and maintain the genetic polymorphism of organisms. Fungal vegetative incompatibility is a type of non-self recognition which often induces programmed cell death (PCD) and restricts the spread of molecular parasites. It is not clearly known whether virus infection could attenuate non-self recognition among host individuals to facilitate its spread. Here, we report that a hypovirulence-associated mycoreovirus, named Sclerotinia sclerotiorum mycoreovirus 4 (SsMYRV4), could suppress host non-self recognition and facilitate horizontal transmission of heterologous viruses. We found that cell death in intermingled colony regions between SsMYRV4-infected Sclerotinia sclerotiorum strain and other tested vegetatively incompatible strains was markedly reduced and inhibition barrage lines were not clearly observed. Vegetative incompatibility, which involves Heterotrimeric guanine nucleotide-binding proteins (G proteins) signaling pathway, is controlled by specific loci termed het (heterokaryon incompatibility) loci. Reactive oxygen species (ROS) plays a key role in vegetative incompatibility-mediated PCD. The expression of G protein subunit genes, het genes, and ROS-related genes were significantly down-regulated, and cellular production of ROS was suppressed in the presence of SsMYRV4. Furthermore, SsMYRV4-infected strain could easily accept other viruses through hyphal contact and these viruses could be efficiently transmitted from SsMYRV4-infected strain to other vegetatively incompatible individuals. Thus, we concluded that SsMYRV4 is capable of suppressing host non-self recognition and facilitating heterologous viruses transmission among host individuals. These findings may enhance our understanding of virus ecology, and provide a potential strategy to utilize hypovirulence-associated mycoviruses to control fungal diseases.

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Section: Resultssupporting

confidence: 79%

Virus-mediated suppression of host non-self recognition facilitates horizontal transmission of heterologous viruses

Chéng

Fù

et al. 2017

PLoS Pathog

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“…It was shown that the pathogen-specific immune defense reaction of the mammary epithelial cell (MEC) 9 determines the ability of the udder to fighting off bacteria 10, 11 . Using MEC it was found in vitro that challenges with E .…”

Section: Introductionmentioning

confidence: 99%

Differentiating Staphylococcus aureus from Escherichia coli mastitis: S. aureus triggers unbalanced immune-dampening and host cell invasion immediately after udder infection

Günther

Petzl²,

Bauer

et al. 2017

Sci Rep

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The etiology determines quality and extent of the immune response after udder infection (mastitis). Infections with Gram negative bacteria (e.g. Escherichia coli) will quickly elicit strong inflammation of the udder, fully activate its immune defence via pathogen receptor driven activation of IκB/NF-κB signaling. This often eradicates the pathogen. In contrast, Gram-positive bacteria (e.g. Staphylococcus aureus) will slowly elicit a much weaker inflammation and immune response, frequently resulting in chronic infections. However, it was unclear which immune regulatory pathways are specifically triggered by S. aureus causing this partial immune subversion. We therefore compared in first lactating cows the earliest (1–3 h) udder responses against infection with mastitis causing pathogens of either species. Global transcriptome profiling, bioinformatics analysis and experimental validation of key aspects revealed as S. aureus infection specific features the (i) failure to activating IκB/NF-κB signaling; (ii) activation of the wnt/β-catenin cascade resulting in active suppression of NF-κB signaling and (iii) rearrangement of the actin-cytoskeleton through modulating Rho GTPase regulated pathways. This facilitates invasion of pathogens into host cells. Hence, S. aureus mastitis is characterized by eliciting unbalanced immune suppression rather than inflammation and invasion of S. aureus into the epithelial cells of the host causing sustained infection.

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“…IHNv is the exception, as this virus is endemic to Sockeye salmon and Rainbow trout populations on the West coast of North America and can cause considerable losses of juvenile (fry-smolt) salmon in freshwater (Wolf, 1988); this virus has also spread to Europe and Asia (Dixon et al , 2016). The level of IHNv impact is highly species-specific.…”

Section: Discussionmentioning

confidence: 99%