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Author Notes:

Arash Grakoui, Ph.D., Emory Vaccine Center, Division of Microbiology and Immunology, Yerkes National Primate Research, Center, Emory University School of Medicine; Division of Infectious Diseases, Department of Medicine, Emory University School of Medicine, 954 Gatewood Road Northeast, Atlanta, GA 30329, Email: arash.grakoui@emory.edu, Tel.: +1-404-727-7822

Disclosures: Nothing to report.

Subjects:

Research Funding:

This project was supported by National Institutes of Health (NIH) grants R01AI136533, R01AI124680, R01AI096882 and R01AI126890 to A.G.; Office of Research Infrastructure Programs/Office of the Director (ORIP/OD) P51OD011132 (formerly National Center For Research Resources (NCRR) P51RR000165) to the Yerkes National Primate Research Center (A.G.) and NIH Institutional Research and Academic Career Development Award (IRACDA) Fellowships in Research and Science Teaching (FIRST) at Emory 5K12GM000680-19 (J.D.S). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Virology
  • CD8(+) T-CELLS
  • DOUBLE-STRANDED-RNA
  • ANTIBODY-RESPONSES
  • VIRAL-HEPATITIS
  • ACTIVATION
  • POTENT
  • PREVALENCE
  • EXPRESSION
  • CLEARANCE
  • THERAPY

Immune system control of hepatitis C virus infection

Tools:

Journal Title:

CURRENT OPINION IN VIROLOGY

Volume:

Volume 46

Publisher:

, Pages 36-44

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Hepatitis C virus (HCV) remains a global public health problem even though more than 95% of infections can be cured by treatment with direct-acting antiviral agents. Resolution of viremia post antiviral therapy does not lead to protective immunity and therefore reinfections can occur. Immune cell detection of HCV activates signaling pathways that produce interferons and trigger the innate immune response against the virus, preventing HCV replication and spread. Cells in the innate immune system, including natural killer, dendritic, and Kupffer cells, interact with infected hepatocytes and present viral antigens to T and B cells where their effector responses contribute to infection outcome. Despite the immune activation, HCV can evade the host response and establish persistent infection. Plans to understand the correlates of protection and strategies to activate proper innate and adaptive immune responses are needed for development of an effective prophylactic vaccine that stimulates protective immunity and limits HCV transmission.

Copyright information:

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (https://creativecommons.org/licenses/by-nc-nd/4.0/rdf).
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