AAM-B Interacts with Nonstructural 4B and Regulates Hepatitis C Virus Propagation
- Authors
- Park, Eun-Mee; Lim, Yun-Sook; Ahn, Byung-Yoon; Hwang, Soon B.
- Issue Date
- 17-7월-2015
- Publisher
- PUBLIC LIBRARY SCIENCE
- Citation
- PLOS ONE, v.10, no.7
- Indexed
- SCIE
SCOPUS
- Journal Title
- PLOS ONE
- Volume
- 10
- Number
- 7
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/92999
- DOI
- 10.1371/journal.pone.0132839
- ISSN
- 1932-6203
- Abstract
- 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.
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