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Effect of inducible expressed human cytomegalovirus immediate early 86 protein on cell apoptosis

Zhiqiang Bai1, Ling Li, Bin Wang

  • 1Department of Microbiology, Key Laboratory of Medicine and Biotechnology of Qingdao, Qingdao University Medical College, Qingdao, Shandong, China.

Bioscience, Biotechnology, and Biochemistry
|June 9, 2009
PubMed

Insights

Human cytomegalovirus IE86 protein inhibits tumor necrosis factor-alpha induced apoptosis, with activity correlating to expression levels. This study developed a Tet-On system for analyzing IE86's role in viral infection.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Human cytomegalovirus (HCMV) is a prevalent pathogen causing severe disease in specific populations.
  • Viral regulatory proteins, including IE72 and IE86, are crucial for HCMV replication within host cells.
  • IE86 significantly influences viral replication, host cell cycle progression, and apoptosis.

Purpose of the Study:

  • To quantify the impact of HCMV IE86 on apoptosis and p53 expression using a Tet-On system.
  • To investigate the relationship between IE86 expression levels and its anti-apoptotic function.
  • To assess the effect of IE86 on p53 mRNA levels during infection.

Main Methods:

  • Utilized a Tet-On inducible gene expression system to control IE86 expression.
  • Quantified apoptosis induction, specifically in response to tumor necrosis factor (TNF)-alpha.
  • Measured p53 mRNA levels to evaluate its regulation by IE86.

Main Results:

  • HCMV IE86 effectively inhibits TNF-alpha-induced apoptosis in host cells.
  • The anti-apoptotic effect of IE86 is dose-dependent, correlating with its expression levels.
  • IE86 expression did not significantly alter the mRNA levels of the p53 gene.

Conclusions:

  • HCMV IE86 possesses significant anti-apoptotic properties, contributing to viral survival.
  • The developed Tet-On system provides a robust platform for functional analysis of HCMV IE86.
  • Understanding IE86's role in apoptosis modulation is vital for comprehending HCMV pathogenesis.

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