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Conditional Immune Escape during Chronic Simian Immunodeficiency Virus Infection.

Dane D Gellerup1, Alexis J Balgeman2, Chase W Nelson3

  • 1Wisconsin National Primate Research Center, University of Wisconsin, Madison, Wisconsin, USA.

Journal of Virology
|October 23, 2015
PubMed
Summary
This summary is machine-generated.

Targeting specific epitopes for anti-HIV CD8 T cell therapies is crucial. Epitopes preserved in heterozygous hosts, unlike homozygous ones, retain immunogenicity, delaying immune escape during chronic simian immunodeficiency virus infection.

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Area of Science:

  • Immunology
  • Virology
  • Genetics

Background:

  • Therapeutic anti-HIV CD8 T cells require targeting epitopes resistant to mutations.
  • Immune escape in T cell epitopes is influenced by host genetics and epitope variation tolerance.
  • Previous work indicated conditional immune escape during acute simian immunodeficiency virus (SIV) infection.

Purpose of the Study:

  • To test if conditional immune escape extends to chronic SIV infection.
  • To determine if preserved epitopes can elicit CD8 T cell responses.
  • To investigate the role of Major Histocompatibility Complex (MHC) heterozygosity in preserving epitope immunogenicity.

Main Methods:

  • Deep sequencing of SIV in Mauritian cynomolgus macaques (MCMs) with M3 MHC homozygous and heterozygous haplotypes.
  • Analysis of epitope variation in relation to MHC genotype.
  • Assessment of chronic CD8 T cell responses against specific epitopes.

Main Results:

  • Epitopes were categorized into three groups (A, B, C) based on variation.
  • Category B epitopes accumulated variants in M3-homozygous MCMs but less so in M3-heterozygous MCMs.
  • Chronic CD8 T cell responses were better preserved in M3-heterozygous MCMs.

Conclusions:

  • Epitopes escaping in MHC-homozygous hosts are preserved and immunogenic in MHC-heterozygous hosts.
  • Heterozygosity delays immune escape, allowing epitopes to retain immunogenicity during chronic infection.
  • The findings support the conditional immune escape hypothesis, highlighting the potential for broader epitope presentation to delay viral escape.