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Measuring Mitochondrial Function of Na&#239;ve and Effector CD8 T Cells
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Reduced eIF3d accelerates HIV disease progression by attenuating CD8+ T cell function.

Ying Pan1,2,3,4, Zi-Ning Zhang1,2,3,4, Lin-Bo Yin1,2,3,4

  • 1NHC Key Laboratory of AIDS Immunology (China Medical University), Department of Laboratory Medicine, The First Affiliated Hospital of China Medical University, No 155, Nanjing North Street, He ping District, Shenyang, Liaoning, 110001, China.

Journal of Translational Medicine
|May 24, 2019
PubMed
Summary
This summary is machine-generated.

Reduced eIF3d expression in early HIV infection is linked to rapid disease progression. This impacts CD8+ T cell function and enhances viral replication, suggesting eIF3d as a potential therapeutic target.

Keywords:
ApoptosisCD8+ T cellsHIVIFN-γProliferationRapid progressorsSOCS-7eIF3d

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Human immunodeficiency virus (HIV) infection can lead to rapid progression in 10-15% of individuals, characterized by a swift decline in CD4+ T cells.
  • Understanding factors influencing rapid disease progression in early HIV infection (EHI) is crucial for timely treatment initiation.
  • Eukaryotic translation initiation factors (eIF3s) regulate mRNA translation and cell function, but their role in HIV prognosis remains unexplored.

Purpose of the Study:

  • To investigate the involvement of eIF3s, specifically eIF3d, in the diverse prognoses of HIV infection.
  • To determine the impact of eIF3d on CD8+ T cell function and HIV replication.
  • To identify potential therapeutic targets for improved immune intervention in HIV infection.

Main Methods:

  • Real-time PCR was used to detect eIF3s expression in cells from HIV-infected patients.
  • RNA sequencing (RNA-Seq) analyzed transcriptomes of eIF3d-inhibited Jurkat T cells.
  • CD8+ T cell proliferation, IFN-γ secretion, and apoptosis were assessed via flow cytometry after eIF3d inhibition (alone or with SOCS-7 knockdown).
  • HIV replication was evaluated in various cell types with eIF3d knockdown using pseudotyped viruses.

Main Results:

  • eIF3d was significantly decreased in rapid progressors (RPs) compared to chronic progressors (CPs) around 100 days post-infection.
  • Reduced eIF3d expression correlated with disease progression in EHI and led to impaired CD8+ T cell proliferation, reduced IFN-γ secretion, and increased apoptosis.
  • Inhibition of eIF3d enhanced SOCS-7 expression; SOCS-7 knockdown rescued CD8+ T cell function.
  • eIF3d inhibition increased HIV replication in Jurkat cells, PBMCs, and CD4+ T cells.

Conclusions:

  • eIF3d plays a critical role in HIV infection by suppressing CD8+ T cell function and promoting viral replication.
  • The findings highlight eIF3d as a potential target for therapeutic strategies aimed at improving immune responses in HIV-infected individuals.