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Human occludin is a hepatitis C virus entry factor required for infection of mouse cells

Author

Listed:
  • Alexander Ploss

    (Center for the Study of Hepatitis C, The Rockefeller University, New York, New York, 10065 USA)

  • Matthew J. Evans

    (Center for the Study of Hepatitis C, The Rockefeller University, New York, New York, 10065 USA
    Present address: Department of Microbiology, Mount Sinai School of Medicine, New York, New York, 10029, USA.)

  • Valeriya A. Gaysinskaya

    (Center for the Study of Hepatitis C, The Rockefeller University, New York, New York, 10065 USA)

  • Maryline Panis

    (Center for the Study of Hepatitis C, The Rockefeller University, New York, New York, 10065 USA)

  • Hana You

    (Center for the Study of Hepatitis C, The Rockefeller University, New York, New York, 10065 USA)

  • Ype P. de Jong

    (Center for the Study of Hepatitis C, The Rockefeller University, New York, New York, 10065 USA
    Mount Sinai School of Medicine, New York, New York, 10029, USA)

  • Charles M. Rice

    (Center for the Study of Hepatitis C, The Rockefeller University, New York, New York, 10065 USA)

Abstract

Hepatitis C: model answer The development of an effective vaccine and specific antiviral therapies against hepatitis C virus (HCV), a leading cause of liver disease, has been hampered by the lack of a convenient small animal model. With the identification of the gap junction protein occludin as the fourth and final key component of the hepatitis C virus cell-entry receptor, that elusive lab model may have come a step nearer. In addition to human occludin, viral infection of murine cells requires expression of the previously identified HCV entry factors CD81, scavenger receptor class B type I, and claudin-1.

Suggested Citation

  • Alexander Ploss & Matthew J. Evans & Valeriya A. Gaysinskaya & Maryline Panis & Hana You & Ype P. de Jong & Charles M. Rice, 2009. "Human occludin is a hepatitis C virus entry factor required for infection of mouse cells," Nature, Nature, vol. 457(7231), pages 882-886, February.
    • Handle: RePEc:nat:nature:v:457:y:2009:i:7231:d:10.1038_nature07684
    DOI: 10.1038/nature07684
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    Cited by:

    1. Mphatso Kalemera & Dilyana Mincheva & Joe Grove & Christopher J R Illingworth, 2019. "Building a mechanistic mathematical model of hepatitis C virus entry," PLOS Computational Biology, Public Library of Science, vol. 15(3), pages 1-26, March.
    2. Pranesh Padmanabhan & Narendra M Dixit, 2011. "Mathematical Model of Viral Kinetics In Vitro Estimates the Number of E2-CD81 Complexes Necessary for Hepatitis C Virus Entry," PLOS Computational Biology, Public Library of Science, vol. 7(12), pages 1-11, December.
    3. Pranesh Padmanabhan & Narendra M Dixit, 2012. "Viral Kinetics Suggests a Reconciliation of the Disparate Observations of the Modulation of Claudin-1 Expression on Cells Exposed to Hepatitis C Virus," PLOS ONE, Public Library of Science, vol. 7(4), pages 1-7, April.
    4. Ashish Kumar & Tiana C. Rohe & Elizabeth J. Elrod & Abdul G. Khan & Altaira D. Dearborn & Ryan Kissinger & Arash Grakoui & Joseph Marcotrigiano, 2023. "Regions of hepatitis C virus E2 required for membrane association," Nature Communications, Nature, vol. 14(1), pages 1-10, December.

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