Hepatitis C virus utilizes VLDLR as a novel entry pathway

Saneyuki Ujino, Hironori Nishitsuji, Takayuki Hishiki, Kazuo Sugiyama, Hiroshi Takaku, Kunitada Shimotohno

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)

Abstract

Various host factors are involved in the cellular entry of hepatitis C virus (HCV). In addition to the factors previously reported, we discovered that the very-low-density lipoprotein receptor (VLDLR) mediates HCV entry independent of CD81. Culturing Huh7.5 cells under hypoxic conditions significantly increased HCV entry as a result of the expression of VLDLR, which was not expressed under normoxic conditions in this cell line. Ectopic VLDLR expression conferred susceptibility to HCV entry of CD81-deficient Huh7.5 cells. Additionally, VLDLR-mediated HCV entry was not affected by the knockdown of cellular factors known to act as HCV receptors or HCV entry factors. Because VLDLR is expressed in primary human hepatocytes, our results suggest that VLDLR functions in vivo as an HCV receptor independent of canonical CD81-mediated HCV entry.

Original languageEnglish
Pages (from-to)188-193
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume113
Issue number1
DOIs
Publication statusPublished - 05-01-2016

All Science Journal Classification (ASJC) codes

  • General

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