Virus and Host Mechanics Support Membrane Penetration and Cell Entry

Greber, Urs F.

doi:10.1128/jvi.02568-15

Cited by 96 publications

(71 citation statements)

References 20 publications

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“…ª 2019 MRC Laboratory of Molecular Biology The EMBO Journal 38: e101365 | 2019 studies in THP-1s have also shown that antibody-containing serum routes AdV into the lysosome (Barlan et al, 2011a). As adenoviruses have membrane lytic capability (Greber, 2016), lysosomal damage resulting from accumulated opsonised AdV has been proposed to trigger NLRP3 activation and IL-1b release in THP-1s (Barlan et al, 2011a). We reasoned that the lysosome may be the destination during increased non-productive viral entry in HMDMs at high IVIg concentrations and that lysosomal damage may be the trigger for the robust IL-1b release we observed at high concentrations of IVIg.…”

Section: Adv-antibody Complex-dependent Il-1b and Tnf Release Can Occmentioning

confidence: 99%

Antibody and DNA sensing pathways converge to activate the inflammasome during primary human macrophage infection

et al. 2019

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Inflammasomes are potent innate immune signalling complexes that couple cytokine release with pro‐inflammatory cell death. However, pathogens have evolved strategies to evade this cell autonomous system. Here, we show how antibodies combine with innate sensors in primary human macrophages to detect viral infection and activate the inflammasome. Our data demonstrate that antibody opsonisation of virions can activate macrophages in multiple ways. In the first, antibody binding of adenovirus causes lysosomal damage, activating NLRP3 to drive inflammasome formation and IL‐1β release. Importantly, this mechanism enhances virion capture but not infection and is accompanied by cell death, denying the opportunity for viral replication. Unexpectedly, we also find that antibody‐coated viruses, which successfully escape into the cytosol, trigger a second system of inflammasome activation. These viruses are intercepted by the cytosolic antibody receptor TRIM21 and the DNA sensor cGAS. Together, these sensors stimulate both NLRP3 inflammasome formation and NFκB activation, driving dose‐dependent IL‐1β and TNF secretion, without inducing cell death. Our data highlight the importance of cooperativity between multiple sensing networks to expose viruses to the inflammasome pathway, which is particularly important for how our innate immune system responds to infection in the presence of pre‐existing immunity.

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Section: Adv-antibody Complex-dependent Il-1b and Tnf Release Can Occmentioning

confidence: 99%

Antibody and DNA sensing pathways converge to activate the inflammasome during primary human macrophage infection

et al. 2019

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“…According to the literature, the viral infection requires a tissue micro-injury, exposing heparin sulfate proteoglycan receptors (Ljubojevic and Skerlev, 2014; Greber, 2016), which are needed for BPV L1 anchorage (Hartl et al , 2011; Buck et al , 2013). , This is confirmed by treatment with heparinase preventing viral infection (Kines et al , 2016).…”

Section: Bpv Infection Pathway and Histopathological Alterationsmentioning

confidence: 99%

Papillomaviruses: a systematic review

et al. 2017

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In the last decades, a group of viruses has received great attention due to its relationship with cancer development and its wide distribution throughout the vertebrates: the papillomaviruses. In this article, we aim to review some of the most relevant reports concerning the use of bovines as an experimental model for studies related to papillomaviruses. Moreover, the obtained data contributes to the development of strategies against the clinical consequences of bovine papillomaviruses (BPV) that have led to drastic hazards to the herds. To overcome the problem, the vaccines that we have been developing involve recombinant DNA technology, aiming at prophylactic and therapeutic procedures. It is important to point out that these strategies can be used as models for innovative procedures against HPV, as this virus is the main causal agent of cervical cancer, the second most fatal cancer in women.

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“…Viruses have evolved sophisticated strategies to penetrate biological membranes to gain entry into host cells and cause disease (Cosset and Lavillette, 2011; Greber, 2016; Luisoni et al, 2015; Dormitzer et al, 2004; Chandran et al, 2002). While membrane penetration by enveloped viruses is reasonably well characterized, the mechanism by which non-enveloped viruses breach a host membrane remains largely enigmatic.…”

Section: Introductionmentioning

confidence: 99%

EMC1-dependent stabilization drives membrane penetration of a partially destabilized non-enveloped virus

Bagchi

Inoue

Tsai

2016

eLife

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Destabilization of a non-enveloped virus generates a membrane transport-competent viral particle. Here we probe polyomavirus SV40 endoplasmic reticulum (ER)-to-cytosol membrane transport, a decisive infection step where destabilization initiates this non-enveloped virus for membrane penetration. We find that a member of the ER membrane protein complex (EMC) called EMC1 promotes SV40 ER membrane transport and infection. Surprisingly, EMC1 does so by using its predicted transmembrane residue D961 to bind to and stabilize the membrane-embedded partially destabilized SV40, thereby preventing premature viral disassembly. EMC1-dependent stabilization enables SV40 to engage a cytosolic extraction complex that ejects the virus into the cytosol. Thus EMC1 acts as a molecular chaperone, bracing the destabilized SV40 in a transport-competent state. Our findings reveal the novel principle that coordinated destabilization-stabilization drives membrane transport of a non-enveloped virus.DOI: http://dx.doi.org/10.7554/eLife.21470.001

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Virus and Host Mechanics Support Membrane Penetration and Cell Entry

Cited by 96 publications

References 20 publications

Antibody and DNA sensing pathways converge to activate the inflammasome during primary human macrophage infection

Antibody and DNA sensing pathways converge to activate the inflammasome during primary human macrophage infection

Papillomaviruses: a systematic review

EMC1-dependent stabilization drives membrane penetration of a partially destabilized non-enveloped virus

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