Doctoral thesis

Immune protection and immune pathogenesis of viral infections

ContributorsRemy, Mélissa
Defense date2013-12-09

Using the model of lymphocytic choriomeningitis virus (LCMV) in mice we have first investigated antiviral antibody protection against persistent infections. We found that neutralization, Fcγ receptor binding and complement activation were dispensable for antiviral antibody protection in vivo. We demonstrated organ-specific effects of antibodies and the absence of neutralization in primary target organs of the virus. Inhibition of infectious virions release from cells might occur, and antiviral protection could be potentiated by inflammation. Secondly, we studied immunopathological mechanisms of Lassa fever (LF) using the new HHD mouse model in which LCMV-WE infection caused a LF-like disease. We showed that T cell activation of virus-infected macrophages triggered the inducible nitric oxide synthase (iNOS) expression in an interferon-γ (IFN-γ) dependent fashion leading to disease. iNOS-deficient or IFN-γ-depleted HHD mice were indeed fully protected, designating nitric oxide as an essential mediator of the terminal disease characterized by systemic edema, circulatory failure and cardioplegia.

  • LCMV
  • Antibody protection
  • Neutralization
  • Fcγ receptors
  • Complement
  • Lassa fever
  • INOS
  • Nitric oxide
  • IFN-γ
Citation (ISO format)
REMY, Mélissa. Immune protection and immune pathogenesis of viral infections. 2013. doi: 10.13097/archive-ouverte/unige:32890
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Creation12/20/2013 11:06:00 AM
First validation12/20/2013 11:06:00 AM
Update time03/14/2023 8:48:36 PM
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