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Analysis of Simian Immunodeficiency Virus-specific CD8+ T-cells in Rhesus Macaques by Peptide-MHC-I Tetramer Staining
Published on: December 23, 2016
Effects of SIVmac infection on peripheral blood CD4+CD8+ T lymphocytes in cynomolgus macaques
1Tsukuba Primate Center, National Institute of Infectious Diseases, Ibaraki, Japan.
Insights
Simian immunodeficiency virus of macaque (SIVmac) infection transiently increases CD4+CD8+ double-positive (DP) T cells in macaques, followed by depletion. The nef gene is crucial for this depletion, suggesting a unique mechanism impacting DP T cell circulation.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- CD4+CD8+ double-positive (DP) T cells with a resting memory phenotype are found in adult cynomolgus macaque peripheral blood.
- Simian immunodeficiency virus of macaque (SIVmac) is a relevant model for studying human immunodeficiency virus (HIV) pathogenesis.
Purpose of the Study:
- To investigate the impact of SIVmac infection on DP T cells in cynomolgus macaques.
- To elucidate the role of the SIVmac nef gene in DP T cell dynamics during infection.
Main Methods:
- In vitro replication assays of SIVmac239 strains in CD4+CD8- and DP T cells.
- Monitoring of DP T cell populations, activation, and viral replication in SIVmac-infected macaques.
- Comparison of infection outcomes between wild-type and nef-deletion mutant SIVmac strains.
Main Results:
- Both wild-type and nef-deletion mutant SIVmac replicated in CD4+CD8- and DP T cells in vitro.
- In vivo, SIVmac infection led to a transient increase and activation of DP T cells, followed by depletion within one month.
- The nef gene was essential for the depletion of DP T cells but not for their initial increase and activation.
Conclusions:
- SIVmac infection alters DP T cell numbers and activation status in macaques.
- The SIVmac nef gene plays a critical role in the depletion of DP T cells, distinct from its role in CD4+CD8- T cell depletion.
- Pathogenic SIV infection may modulate DP T cell production or circulation via Nef-dependent mechanisms.
Abstract:
We have previously reported that CD4+CD8+ double-positive (DP) T cells with a resting memory phenotype exist in a substantial proportion of peripheral blood lymphocytes of adult cynomolgus macaques. In this study, we examined the effects of simian immunodeficiency virus of macaque (SIVmac) infection on DP T cells. In vitro, SIVmac239 nef-open (239) and its nef-deletion mutant replicated well in both CD4+CD8- and DP T cells. However, when the macaques were infected with 239, DP, but not CD4+CD8-, T cells were transiently increased in parallel with cell activation and viral replication, followed by depletion within 1 month postinfection. Interestingly, the nef gene was required for depletion but not for the increase and activation of DP T cells. These data suggest that the pathogenic SIV infection may downmodulate production and/or blood circulation of DP T cells by a Nef function-related mechanism(s) different from that for the depletion of CD4+CD8- T cells.
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