Hepatitis C virus utilizes VLDLR as a novel entry pathway.
basic_science · Level V
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- Record sourced from PubMed, PMID 26699506.
- Also identified by DOI 10.1073/pnas.1506524113 and PMC identifier 4711846.
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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.
Medical subject headings
- Hepacivirus
- Hepatitis C
- Hepatocytes
- Receptors, LDL
- Receptors, Virus
- Virus Internalization