293 Cells over-expressing human ADI1 and CD81 are permissive for serum-derived hepatitis C virus infection

Ju Chien Cheng, Yung Ju Yeh, Li Mei Pai, Ming Ling Chang, Chau Ting Yeh*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

12 Scopus citations

Abstract

Human aci-reductone dioxygenase 1 (ADI1) is a member of the Cupin superfamily. It binds to and inhibits the activities of membrane-type 1 matrix metalloproteinase, a protein known to interact with the tight junction protein, claudin-1. Previously, a variant protein, named submergenceinduced protein-like factor (Sip-L), consisting of ADI1 amino acids 64-179, was found to support hepatitis C virus (HCV) infection and replication in 293 cells. In the present study, it was discovered that over-expression of human ADI1 in 293 cells (293-ADI1 cells) also supported HCV infection and replication. Using serum-derived HCV as an infectious source, enhanced cell uptake of HCV to a Northern blot detectable level was found in 293 cells over-expressing both CD81 and ADI1 (293-ADI1-CD81 cells). The enhanced cell entry was confirmed by the use of the vesicular stomatitis virus-basedHCVpseudotype particles. However, transfection of HCV replicon RNA by electroporation into naïve 293 and 293-ADI1 cells revealed no difference in replication efficiency. Using the infectious J6/JFH chimera as an infectious source, the infectivity was compared between 293-ADI1-CD81 and Huh-7.5 cells. More infection foci were formed in the 293-ADI1-CD81 cells in the first round of infection. In conclusion, human ADI1 over-expression in 293 cells enhances cell entry but not replication of HCV. 293-ADI1-CD81 cells are permissive for serum-derived HCV infection.

Original languageEnglish
Pages (from-to)1560-1568
Number of pages9
JournalJournal of Medical Virology
Volume81
Issue number9
DOIs
StatePublished - 09 2009

Keywords

  • Cell entry
  • Claudin-1
  • Membrane-type 1 matrix metalloproteinase

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