AAM-B interacts with nonstructural 4B and regulates hepatitis C virus propagation

Eun Mee Park, Yun Sook Lim, Byung Yoon Ahn, Soon B. Hwang

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)


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.

Original languageEnglish
Article number132839
JournalPloS one
Issue number7
Publication statusPublished - 2015 Jul 17

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • General


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