Modification of intracellular membrane structures for virus replication

Miller, Sven; Krijnse‐Locker, Jacomine

doi:10.1038/nrmicro1890

Cited by 653 publications

(662 citation statements)

References 115 publications

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“…SFV replication intermediates) might be poor substrates for Dicer due to intrinsic features (e.g. 5′ cap modifications) or due to the fact that they are sequestered inside membrane‐bound replication complexes (“viral factories”) (Miller & Krijnse‐Locker, 2008; den Boon & Ahlquist, 2010). Alternatively, the amplitude and/or kinetics of the dsRNAi response upon virus infection and/or the amount of dsRNA substrate produced by viral replication might not be sufficient to provide effective antiviral protection in the cell types that we studied.…”

Section: Discussionmentioning

confidence: 99%

Inactivation of the type I interferon pathway reveals long double‐stranded RNA‐mediated RNA interference in mammalian cells

et al. 2016

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RNA interference (RNAi) elicited by long double‐stranded (ds) or base‐paired viral RNA constitutes the major mechanism of antiviral defence in plants and invertebrates. In contrast, it is controversial whether it acts in chordates. Rather, in vertebrates, viral RNAs induce a distinct defence system known as the interferon (IFN) response. Here, we tested the possibility that the IFN response masks or inhibits antiviral RNAi in mammalian cells. Consistent with that notion, we find that sequence‐specific gene silencing can be triggered by long dsRNAs in differentiated mouse cells rendered deficient in components of the IFN pathway. This unveiled response is dependent on the canonical RNAi machinery and is lost upon treatment of IFN‐responsive cells with type I IFN. Notably, transfection with long dsRNA specifically vaccinates IFN‐deficient cells against infection with viruses bearing a homologous sequence. Thus, our data reveal that RNAi constitutes an ancient antiviral strategy conserved from plants to mammals that precedes but has not been superseded by vertebrate evolution of the IFN system.

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Section: Discussionmentioning

confidence: 99%

Inactivation of the type I interferon pathway reveals long double‐stranded RNA‐mediated RNA interference in mammalian cells

et al. 2016

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“…This burst of viral protein expression is general to all viruses. In the case of vaccinia virus and its MVA derivative, a likely additional mechanism is that these viruses, as many others, generate their own replication center in the cytoplasm and recruit endoplasmic reticulum membranes to this structure (37). It is therefore possible that endogenous MHC class I molecules that are inserted upon cotranslational translocation into endoplasmic reticulum membranes surrounding a viral replication center will likely be confronted with virally derived peptides.…”

Section: Discussionmentioning

confidence: 99%

Cognate Peptide–MHC Complexes Are Expressed as Tightly Apposed Nanoclusters in Virus-Infected Cells To Allow TCR Crosslinking

Ferez

Castro

Alarcón

et al. 2014

The Journal of Immunology

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Antigenic T cell stimulation requires interaction between the TCR of the T cell and cognate peptide–MHC molecules presented by the APC. Although studies with TCR-specific Abs and soluble peptide–MHC ligands have shown that the TCR needs to be crosslinked by two or more ligands to induce T cell stimulation, it is not understood how several MHC molecules loaded with the cognate antigenic peptide can produce crosslinking under physiological conditions. We show at the molecular level that large clusters of cognate peptide–MHC are formed at the surface of murine professional and nonprofessional APCs upon virus infection and that these clusters impinge on the stimulatory capacity of the APC. These clusters are formed by tight apposition of cognate peptide–MHC complexes in a configuration that is compatible with simultaneous engagement of two or more TCRs. This suggests that physiological expression of Ag allows formation of multivalent ligands for the TCR that permit TCR crosslinking and T cell activation.

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“…The process of endocytosis is vital in a variety of pathophysiological phenomena, including substance uptake, receptor down regulation, microbial infection, and phagocytosis of apoptotic cells [32][33][34]. Diverse molecules have been implicated in the machinery related to endocytosis, and disruption of this machinery results in various disorders, including the loss of epithelial polarity and barrier functions [35,36].…”

Section: Discussionmentioning

confidence: 99%