Persistent Zika Virus Clinical Susceptibility despite Reduced Viral Burden in Mice with Expanded Virus-Specific CD8+ T Cells Primed by Recombinant Listeria monocytogenes

J Immunol. 2020 Jul 15;205(2):447-453. doi: 10.4049/jimmunol.1901412. Epub 2020 Jun 10.

Abstract

Vaccines against Zika virus (ZIKV) infection that target CD8+ T cells are of considerable interest because Abs may enhance infection susceptibility. However, whether CD8+ T cells are protective or promote susceptibility to clinical infection symptoms remains uncertain. To more precisely investigate ZIKV-specific CD8+ T cells in isolation, we engineered a Listeria monocytogenes-based vector to express a single MHC class I-restricted immune dominant peptide, E294-302, from ZIKV envelope protein. We show accumulation of activated ZIKV-specific CD8+ T cells primed by recombinant L. monocytogenes is associated with reductions in circulating virus levels after ZIKV challenge in type I IFN receptor-deficient mice and wildtype mice administered neutralizing Abs against type I IFN receptor. Interestingly, susceptibility to ZIKV clinical infection including weight loss and mortality each persists and is neither significantly improved nor worsened compared with isogenic L. monocytogenes-primed control mice. These data demonstrating persistent ZIKV clinical susceptibility despite reduced viral burden in mice with expanded virus-specific CD8+ T cells highlights the need for targeting other adaptive immune components in developing vaccines against ZIKV infection.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Blocking / administration & dosage
  • CD8-Positive T-Lymphocytes / immunology*
  • Cells, Cultured
  • Disease Resistance
  • Disease Susceptibility
  • Humans
  • Listeria monocytogenes / physiology*
  • Listeriosis / immunology*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Peptides / immunology
  • Receptor, Interferon alpha-beta / genetics
  • Receptor, Interferon alpha-beta / metabolism*
  • Viral Envelope Proteins / immunology
  • Viral Load
  • Zika Virus / physiology*
  • Zika Virus Infection / immunology*

Substances

  • Antibodies, Blocking
  • Ifnar1 protein, mouse
  • Peptides
  • Viral Envelope Proteins
  • Receptor, Interferon alpha-beta