Human Rhinovirus 16 Causes Golgi Apparatus Fragmentation without Blocking Protein Secretion
The replication of picornaviruses has been described to cause fragmentation of the Golgi apparatus that blocks the secretory pathway. The inhibition of major histocompatibility complex class I upregulation and cytokine, chemokine and interferon secretion may have important implications for host defe...
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American Society for Microbiology
2014
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pubmed-41787212015-04-01 Human Rhinovirus 16 Causes Golgi Apparatus Fragmentation without Blocking Protein Secretion Mousnier, Aurelie Swieboda, Dawid Pinto, Anaïs Guedán, Anabel Rogers, Andrew V. Walton, Ross Johnston, Sebastian L. Solari, Roberto Virus-Cell Interactions The replication of picornaviruses has been described to cause fragmentation of the Golgi apparatus that blocks the secretory pathway. The inhibition of major histocompatibility complex class I upregulation and cytokine, chemokine and interferon secretion may have important implications for host defense. Previous studies have shown that disruption of the secretory pathway can be replicated by expression of individual nonstructural proteins; however the situation with different serotypes of human rhinovirus (HRV) is unclear. The expression of 3A protein from HRV14 or HRV2 did not cause Golgi apparatus disruption or a block in secretion, whereas other studies showed that infection of cells with HRV1A did cause Golgi apparatus disruption which was replicated by the expression of 3A. HRV16 is the serotype most widely used in clinical HRV challenge studies; consequently, to address the issue of Golgi apparatus disruption for HRV16, we have systematically and quantitatively examined the effect of HRV16 on both Golgi apparatus fragmentation and protein secretion in HeLa cells. First, we expressed each individual nonstructural protein and examined their cellular localization and their disruption of endoplasmic reticulum and Golgi apparatus architecture. We quantified their effects on the secretory pathway by measuring secretion of the reporter protein Gaussia luciferase. Finally, we examined the same outcomes following infection of cells with live virus. We demonstrate that expression of HRV16 3A and 3AB and, to a lesser extent, 2B caused dispersal of the Golgi structure, and these three nonstructural proteins also inhibited protein secretion. The infection of cells with HRV16 also caused significant Golgi apparatus dispersal; however, this did not result in the inhibition of protein secretion. American Society for Microbiology 2014-10 /pmc/articles/PMC4178721/ /pubmed/25100828 http://dx.doi.org/10.1128/JVI.01170-14 Text en Copyright © 2014 Mousnier et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution 3.0 Unported license (http://creativecommons.org/licenses/by/3.0/) . |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Mousnier, Aurelie Swieboda, Dawid Pinto, Anaïs Guedán, Anabel Rogers, Andrew V. Walton, Ross Johnston, Sebastian L. Solari, Roberto |
spellingShingle |
Mousnier, Aurelie Swieboda, Dawid Pinto, Anaïs Guedán, Anabel Rogers, Andrew V. Walton, Ross Johnston, Sebastian L. Solari, Roberto Human Rhinovirus 16 Causes Golgi Apparatus Fragmentation without Blocking Protein Secretion |
author_facet |
Mousnier, Aurelie Swieboda, Dawid Pinto, Anaïs Guedán, Anabel Rogers, Andrew V. Walton, Ross Johnston, Sebastian L. Solari, Roberto |
author_sort |
Mousnier, Aurelie |
title |
Human Rhinovirus 16 Causes Golgi Apparatus Fragmentation without Blocking Protein Secretion |
title_short |
Human Rhinovirus 16 Causes Golgi Apparatus Fragmentation without Blocking Protein Secretion |
title_full |
Human Rhinovirus 16 Causes Golgi Apparatus Fragmentation without Blocking Protein Secretion |
title_fullStr |
Human Rhinovirus 16 Causes Golgi Apparatus Fragmentation without Blocking Protein Secretion |
title_full_unstemmed |
Human Rhinovirus 16 Causes Golgi Apparatus Fragmentation without Blocking Protein Secretion |
title_sort |
human rhinovirus 16 causes golgi apparatus fragmentation without blocking protein secretion |
description |
The replication of picornaviruses has been described to cause fragmentation of the Golgi apparatus that blocks the secretory pathway. The inhibition of major histocompatibility complex class I upregulation and cytokine, chemokine and interferon secretion may have important implications for host defense. Previous studies have shown that disruption of the secretory pathway can be replicated by expression of individual nonstructural proteins; however the situation with different serotypes of human rhinovirus (HRV) is unclear. The expression of 3A protein from HRV14 or HRV2 did not cause Golgi apparatus disruption or a block in secretion, whereas other studies showed that infection of cells with HRV1A did cause Golgi apparatus disruption which was replicated by the expression of 3A. HRV16 is the serotype most widely used in clinical HRV challenge studies; consequently, to address the issue of Golgi apparatus disruption for HRV16, we have systematically and quantitatively examined the effect of HRV16 on both Golgi apparatus fragmentation and protein secretion in HeLa cells. First, we expressed each individual nonstructural protein and examined their cellular localization and their disruption of endoplasmic reticulum and Golgi apparatus architecture. We quantified their effects on the secretory pathway by measuring secretion of the reporter protein Gaussia luciferase. Finally, we examined the same outcomes following infection of cells with live virus. We demonstrate that expression of HRV16 3A and 3AB and, to a lesser extent, 2B caused dispersal of the Golgi structure, and these three nonstructural proteins also inhibited protein secretion. The infection of cells with HRV16 also caused significant Golgi apparatus dispersal; however, this did not result in the inhibition of protein secretion. |
publisher |
American Society for Microbiology |
publishDate |
2014 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4178721/ |
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1613138588323545088 |