Receptor Complementation and Mutagenesis Reveal SR-BI as an Essential HCV Entry Factor and Functionally Imply Its Intra- and Extra-Cellular Domains
2009

SR-BI: A Key Player in Hepatitis C Virus Entry

publication 10 minutes Evidence: high

Author Information

Author(s): Dreux Marlène, Dao Thi Viet Loan, Fresquet Judith, Guérin Maryse, Julia Zélie, Verney Géraldine, Durantel David, Zoulim Fabien, Lavillette Dimitri, Cosset François-Loïc, Bartosch Birke

Primary Institution: Université de Lyon, UCB-Lyon1, IFR128; INSERM, U758; Ecole Normale Supérieure de Lyon, Lyon, France

Hypothesis

Is SR-BI an essential factor for HCV entry into cells?

Conclusion

The study demonstrates that SR-BI is an essential entry factor for HCV, influencing both binding and infection enhancement through lipid transfer.

Supporting Evidence

  • SR-BI is required for HCV entry, as shown by complementation assays.
  • Mutations in SR-BI affect its ability to mediate HCV entry.
  • HDL enhances HCV entry through SR-BI, indicating a functional role in infection.

Takeaway

SR-BI helps the hepatitis C virus get into cells, and it does this by grabbing onto the virus and using lipids to make the entry easier.

Methodology

The study used complementation assays in various cell lines to assess the role of SR-BI in HCV entry, including mutagenesis of SR-BI to identify functional domains.

Limitations

The study primarily focused on specific cell lines, which may not fully represent all human tissues.

Digital Object Identifier (DOI)

10.1371/journal.ppat.1000310

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication