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CD59 incorporation protects hepatitis C virus against complement-mediated destruction
Tohti Amet1, Marwan Ghabril, Naga Chalasani
1Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Hepatology (Baltimore, Md.)
|September 21, 2011
Summary
Hepatitis C virus (HCV) incorporates host CD59 protein into its envelope, evading immune attack. Blocking CD59 makes HCV vulnerable to complement-mediated lysis, suggesting a new therapeutic target for HCV infection.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Enveloped viruses like HIV-1 and influenza evade immune responses by incorporating host regulators of complement activation (RCA).
- Hepatitis C virus (HCV) chronically infects patients despite neutralizing antibodies, suggesting immune evasion strategies.
- CD59 is a key RCA member known to protect cells from complement-mediated damage.
Purpose of the Study:
- To investigate whether Hepatitis C virus (HCV) virions incorporate biologically functional CD59.
- To determine if CD59 incorporation aids HCV in escaping antibody-dependent complement-mediated lysis (ADCML).
Main Methods:
- Detection of CD59 on HCV particles using CD59-specific antibodies and immunoblot analysis.
- Enzyme-linked immunosorbent assay (ELISA) to quantify CD59 in purified HCV and cell supernatants.
- Assessing HCV sensitivity to ADCML after blocking CD59 function.
Main Results:
- CD59 was found associated with the external membrane of HCV particles from cell lines and patient plasma.
- Purified HCV particles and supernatants from infected cells showed detectable CD59.
- Blocking CD59 increased HCV sensitivity to ADCML and reduced viral infectivity.
- Adding CD59 blockers to patient plasma enhanced autologous virolysis.
Conclusions:
- CD59 is incorporated into HCV virions, providing protection against antibody-dependent complement-mediated lysis (ADCML).
- This study is the first to demonstrate CD59's role in HCV immune evasion.
- Blocking CD59 in patient plasma sensitizes circulating HCV virions to complement-mediated attack, indicating therapeutic potential.
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