AAM-B Interacts with Nonstructural 4B and Regulates Hepatitis C Virus Propagation.
Hepatitis C virus (HCV) usurps host cellular lipid metabolism for production of infectious virus particles. Recently, we have screened a siRNA library targeting host factors that control lipid metabolism and lipid droplet (LD) formation in cell culture grown HCV (HCVcc)-infected cells. Of 10 final c...
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doaj-fd7ddf2665214432811fd9831024dc972020-11-25T01:21:40ZengPublic Library of Science (PLoS)PLoS ONE1932-62032015-01-01107e013283910.1371/journal.pone.0132839AAM-B Interacts with Nonstructural 4B and Regulates Hepatitis C Virus Propagation.Eun-Mee ParkYun-Sook LimByung-Yoon AhnSoon B HwangHepatitis C virus (HCV) usurps host cellular lipid metabolism for production of infectious virus particles. Recently, we have screened a siRNA library targeting host factors that control lipid metabolism and lipid droplet (LD) formation in cell culture grown HCV (HCVcc)-infected cells. Of 10 final candidates, we selected the gene encoding AAM-B for further characterization. We showed that siRNA-mediated knockdown of AAM-B impaired HCV propagation in Jc1-infected cells. More precisely, knockdown of AAM-B abrogated production of infectious HCV particles in both Jc1 RNA electroporated cells and Jc1-infected cells. It is worth noting that knockdown of AAM-B exerted no effect on lipid droplet formation. Moreover, AAM-B interacted with nonstructural 4B (NS4B) through the C-terminal region of NS4B. Protein interplay between AAM-B and NS4B was verified in the context of HCV replication. Using either transient or stable expression of AAM-B, we verified that AAM-B colocalized with NS4B in the cytoplasm. Immunofluorescence data further showed that AAM-B might be involved in recruitment of NS4B to sites in close proximity to LDs to facilitate HCV propagation. Collectively, this study provides new insight into how HCV utilizes cellular AAM-B to facilitate viral propagation.http://europepmc.org/articles/PMC4505943?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Eun-Mee Park Yun-Sook Lim Byung-Yoon Ahn Soon B Hwang |
spellingShingle |
Eun-Mee Park Yun-Sook Lim Byung-Yoon Ahn Soon B Hwang AAM-B Interacts with Nonstructural 4B and Regulates Hepatitis C Virus Propagation. PLoS ONE |
author_facet |
Eun-Mee Park Yun-Sook Lim Byung-Yoon Ahn Soon B Hwang |
author_sort |
Eun-Mee Park |
title |
AAM-B Interacts with Nonstructural 4B and Regulates Hepatitis C Virus Propagation. |
title_short |
AAM-B Interacts with Nonstructural 4B and Regulates Hepatitis C Virus Propagation. |
title_full |
AAM-B Interacts with Nonstructural 4B and Regulates Hepatitis C Virus Propagation. |
title_fullStr |
AAM-B Interacts with Nonstructural 4B and Regulates Hepatitis C Virus Propagation. |
title_full_unstemmed |
AAM-B Interacts with Nonstructural 4B and Regulates Hepatitis C Virus Propagation. |
title_sort |
aam-b interacts with nonstructural 4b and regulates hepatitis c virus propagation. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2015-01-01 |
description |
Hepatitis C virus (HCV) usurps host cellular lipid metabolism for production of infectious virus particles. Recently, we have screened a siRNA library targeting host factors that control lipid metabolism and lipid droplet (LD) formation in cell culture grown HCV (HCVcc)-infected cells. Of 10 final candidates, we selected the gene encoding AAM-B for further characterization. We showed that siRNA-mediated knockdown of AAM-B impaired HCV propagation in Jc1-infected cells. More precisely, knockdown of AAM-B abrogated production of infectious HCV particles in both Jc1 RNA electroporated cells and Jc1-infected cells. It is worth noting that knockdown of AAM-B exerted no effect on lipid droplet formation. Moreover, AAM-B interacted with nonstructural 4B (NS4B) through the C-terminal region of NS4B. Protein interplay between AAM-B and NS4B was verified in the context of HCV replication. Using either transient or stable expression of AAM-B, we verified that AAM-B colocalized with NS4B in the cytoplasm. Immunofluorescence data further showed that AAM-B might be involved in recruitment of NS4B to sites in close proximity to LDs to facilitate HCV propagation. Collectively, this study provides new insight into how HCV utilizes cellular AAM-B to facilitate viral propagation. |
url |
http://europepmc.org/articles/PMC4505943?pdf=render |
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