Deciphering Virus Entry with Fluorescently Labeled Viral Particles

Hoffmann, Anja; Mazelier, Magalie; Léger, Psylvia; Lozach, Pierre‐Yves

doi:10.1007/978-1-4939-8678-1_8

Cited by 23 publications

(25 citation statements)

References 39 publications

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“…However, after the attachment of virions to their receptor(s), the process of passage from the outside to the inside of the cell remains to be discovered for most phenuiviruses ( Figure 2 ). By combining the use of fluorescently-labeled UUKV particles [ 57 ] and the expression of green fluorescent protein-tagged DC-SIGN molecules, it was possible to visualize virus-receptor interactions in living cells for the first time [ 41 ]. This model has made it possible to analyze the dynamics of these interactions and, in particular, to observe the recruitment of receptor molecules to the UUKV binding site on the cell surface [ 41 ].…”

Section: Internalization Of Phenuiviruses Into Cellsmentioning

confidence: 99%

Entry of Phenuiviruses into Mammalian Host Cells

Koch

Xin

Tischler

et al. 2021

Viruses

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Phenuiviridae is a large family of arthropod-borne viruses with over 100 species worldwide. Several cause severe diseases in both humans and livestock. Global warming and the apparent geographical expansion of arthropod vectors are good reasons to seriously consider these viruses potential agents of emerging diseases. With an increasing frequency and number of epidemics, some phenuiviruses represent a global threat to public and veterinary health. This review focuses on the early stage of phenuivirus infection in mammalian host cells. We address current knowledge on each step of the cell entry process, from virus binding to penetration into the cytosol. Virus receptors, endocytosis, and fusion mechanisms are discussed in light of the most recent progress on the entry of banda-, phlebo-, and uukuviruses, which together constitute the three prominent genera in the Phenuiviridae family.

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Section: Internalization Of Phenuiviruses Into Cellsmentioning

confidence: 99%

Entry of Phenuiviruses into Mammalian Host Cells

Koch

Xin

Tischler

et al. 2021

Viruses

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“…IAV X31 was labelled with Alexa Fluor 488 (Thermo Fisher Scientific) as described (Hoffmann et al, 2018). IAV entry assays were performed as previously described (Banerjee et al, 2013;Banerjee et al, 2014;Miyake et al, 2019).…”

Section: Iav Binding and Endocytosis Assaymentioning

confidence: 99%

Non‐canonical autophagy functions of ATG16L1 in epithelial cells limit lethal infection by influenza A virus

et al. 2021

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Influenza A virus (IAV) and SARS-CoV-2 (COVID-19) cause pandemic infections where cytokine storm syndrome and lung inflammation lead to high mortality. Given the high social and economic cost of respiratory viruses, there is an urgent need to understand how the airways defend against virus infection. Here we use mice lacking the WD and linker domains of ATG16L1 to demonstrate that ATG16L1dependent targeting of LC3 to single-membrane, non-autophagosome compartmentsreferred to as non-canonical autophagyprotects mice from lethal IAV infection. Mice with systemic loss of non-canonical autophagy are exquisitely sensitive to low-pathogenicity IAV where extensive viral replication throughout the lungs, coupled with cytokine amplification mediated by plasmacytoid dendritic cells, leads to fulminant pneumonia, lung inflammation and high mortality. IAV was controlled within epithelial barriers where non-canonical autophagy reduced IAV fusion with endosomes and activation of interferon signalling. Conditional mouse models and ex vivo analysis showed that protection against IAV infection of lung was independent of phagocytes and other leucocytes. This establishes non-canonical autophagy in airway epithelial cells as a novel innate defence that restricts IAV infection and lethal inflammation at respiratory surfaces.

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“…6A). To assess virus uptake into A549 cells, a flow cytometry-based assay was used to distinguish virus particles at the plasma membrane from those which were internalized (41). This assay relies on the biochemical property of the membrane-impermeable dye, trypan blue, that quenches the fluorescence emitted by UUKV- min after temperature shift, no significant difference was observed between GBF1 silenced and the control cells (Fig.…”

Section: Gbf1 Is Critical For Uukv Replication and Infectious Particlmentioning

confidence: 99%

Quantitative Proteomics of Uukuniemi Virus-host Cell Interactions Reveals GBF1 as Proviral Host Factor for Phleboviruses

Uckeley

Moeller

Kühn

et al. 2019

Molecular & Cellular Proteomics

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Novel tick-borne phleboviruses in the Phenuiviridae family, which are highly pathogenic in humans and all closely related to Uukuniemi virus (UUKV), have recently emerged on different continents. How phleboviruses assemble, bud, and exit cells remains largely elusive. Here, we performed high-resolution, label-free mass spectrometry analysis of UUKV immuno-precipitated from cell lysates and identified 39 cellular partners interacting with the viral envelope glycoproteins. The importance of these host factors for UUKV infection was validated by silencing each host factor by RNA interference. This revealed Golgi-specific brefeldin Aresistance guanine nucleotide exchange factor 1 (GBF1), a guanine nucleotide exchange factor resident in the Golgi, as a critical host factor required for the UUKV life cycle. An inhibitor of GBF1, Golgicide A, confirmed the role of the cellular factor in UUKV infection. We could pinpoint the GBF1 requirement to UUKV replication and particle assembly. When the investigation was extended to viruses from various positive and negative RNA viral families, we found that not only phleboviruses rely on GBF1 for infection, but also Flavi-, Corona-, Rhabdo-, and Togaviridae. In contrast, silencing or blocking GBF1 did not abrogate infection by the human adenovirus serotype 5 and immunodeficiency retrovirus type 1, the replication of both occurs in the nucleus. Together our results indicate that UUKV relies on GBF1 for viral replication, assembly and egress. This study also highlights the proviral activity of GBF1 in the infection by a broad range of important zoonotic RNA viruses.

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Deciphering Virus Entry with Fluorescently Labeled Viral Particles

Cited by 23 publications

References 39 publications

Entry of Phenuiviruses into Mammalian Host Cells

Entry of Phenuiviruses into Mammalian Host Cells

Non‐canonical autophagy functions of ATG16L1 in epithelial cells limit lethal infection by influenza A virus

Quantitative Proteomics of Uukuniemi Virus-host Cell Interactions Reveals GBF1 as Proviral Host Factor for Phleboviruses

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