The entry of HCV into host cells involves a variety of host factors; CD81 in particular has a critical role. However, the authors of a new study have reported that Huh7.5 cells cultured under hypoxic conditions demonstrated increased HCV entry as a result of expression of very-low-density lipoprotein receptor (VLDLR). Furthermore, ectopic VLDLR expression conferred susceptibility to HCV entry of CD81-deficient Huh7.5 cells. VLDLR might represent a novel HCV entry pathway, independent of CD81.
Change history
17 February 2016
In the version of the In Brief article initially published online and in print, the original article reference “Racaniello, V, et al. Hepatitis C virus utilizes VLDLR as a novel entry pathway. Proc. Natl Acad. Sci. USA 113, 188–193 (2016)” was incorrect and should have read “Ujino, S. et al. Hepatitis C virus utilizes VLDLR as a novel entry pathway. Proc. Natl Acad. Sci. USA 113, 188–193 (2016)”.
References
Ujino, S, et al. Hepatitis C virus utilizes VLDLR as a novel entry pathway. Proc. Natl Acad. Sci. USA 113, 188–193 (2016)
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New entry pathway for HCV. Nat Rev Gastroenterol Hepatol 13, 64 (2016). https://doi.org/10.1038/nrgastro.2016.11
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DOI: https://doi.org/10.1038/nrgastro.2016.11
