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Transcription Factor ZNF683 Inhibits SIV/HIV Replication through Regulating IFNγ Secretion of CD8+ T Cells

Ying Lu1,2, Ming-Xu Zhang1, Wei Pang1

  • 1Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China.

Viruses
|April 23, 2022
PubMed

Insights

Researchers identified distinct lung microbial patterns and higher ZNF683 expression in slow-progressing AIDS models. ZNF683 enhances CD8+ T cell function, potentially slowing human immunodeficiency virus (HIV) replication.

Area of Science:

  • Immunology
  • Microbiology
  • Virology

Background:

  • Pulmonary microbial invasion and inflammatory cytokines are key factors in human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) progression.
  • Distinct rates of AIDS progression are observed in HIV patients, suggesting underlying molecular differences.
  • Northern pig-tailed macaques (NPMs) infected with SIVmac239 serve as a relevant model for studying AIDS pathogenesis, exhibiting rapid progressor (RP) and slow progressor (SP) phenotypes.

Purpose of the Study:

  • To investigate the molecular mechanisms differentiating rapid versus slow AIDS progression in an SIVmac239-infected macaque model.
  • To identify microbial and host molecular differences in the lungs associated with varying disease progression rates.

Main Methods:

  • Utilized 16S rDNA sequencing to analyze pulmonary microbial communities in rapid progressor (RP) and slow progressor (SP) macaques.
  • Employed transcriptome sequencing of lung tissue to assess host gene expression profiles.
  • Conducted functional experiments to evaluate the role of identified molecular factors, such as ZNF683, in immune cell function and viral replication.

Main Results:

  • Significant differences in pulmonary microbial composition were observed between RP and SP groups, with distinct marker flora including Family XI, Enterococcus, Ezakiella, and increased Lactobacilli in RPs.
  • Pulmonary transcriptome analysis revealed significantly higher expression of the transcription factor ZNF683 in the SP group compared to the RP group.
  • Functional experiments demonstrated that ZNF683 enhances CD8+ T cell proliferation and interferon-gamma (IFNγ) secretion, correlating with decreased SIV/HIV replication.

Conclusions:

  • ZNF683 plays a crucial role in enhancing CD8+ T cell responses, potentially contributing to slower AIDS progression by inhibiting viral replication.
  • Distinct pulmonary microbial profiles and host gene expression, particularly ZNF683, are associated with differential AIDS progression rates in SIV-infected macaques.
  • These findings offer insights into the complex interplay of microbial and host factors governing HIV/AIDS pathogenesis and progression.
Keywords:
SIVmac239ZNF683lungnorthern pig-tailed macaquesrapid progressorsslow progressors

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