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Related Experiment Videos

Epstein-barr virus-induced changes in B-lymphocyte gene expression.

Kara L Carter1, Ellen Cahir-McFarland, Elliott Kieff

  • 1The Channing Laboratory, Brigham and Women's Hospital, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA.

Journal of Virology
|September 20, 2002
PubMed
Summary

Epstein-Barr virus (EBV) infection significantly alters B lymphocyte gene expression during latency III. This study identified novel EBV-induced and repressed genes critical for transforming B cells into lymphoblastoid cell lines (LCLs).

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Area of Science:

  • Molecular Virology
  • Immunology
  • Cell Biology

Background:

  • Epstein-Barr virus (EBV) latency III gene expression is crucial for transforming primary B lymphocytes into lymphoblastoid cell lines (LCLs).
  • Understanding the molecular mechanisms underlying this transformation requires detailed analysis of cellular gene expression changes induced by EBV.

Purpose of the Study:

  • To elucidate the mechanisms of EBV latency III-mediated transformation of B lymphocytes by assessing associated gene expression alterations.
  • To identify novel EBV-induced and repressed genes involved in B cell transformation.

Main Methods:

  • Utilized microarray analysis of 4,146 cellular cDNAs to compare gene expression in EBV-infected and uninfected B cell lines (BL41, BL41EBV, IB4 LCLs).
  • Employed real-time reverse transcription-PCR (RT-PCR) to confirm and validate the expression levels of newly identified EBV-regulated genes.

Related Experiment Videos

  • Investigated promoter regions of identified genes to infer potential mediating transcription factors (NF-kappaB, PU.1) and EBV proteins (LMP1, EBNA2).

    • Main Results:

    • Microarray analysis detected 1,405 cDNAs, with 38 RNAs consistently upregulated in EBV-infected LCLs compared to uninfected cells.
    • Confirmed 23 newly identified EBV-induced genes and identified nine newly identified EBV-repressed genes, including CD10.
    • EBV-regulated genes are involved in critical cellular processes such as signal transduction, transcription, protein metabolism, and cell adhesion.

    Conclusions:

    • EBV latency III infection profoundly alters B lymphocyte gene expression, driving the transformation process.
    • Newly identified EBV-regulated genes play significant roles in LCL formation and function.
    • NF-kappaB and PU.1, potentially mediated by LMP1 and EBNA2, are implicated as key players in EBV-driven B cell alterations.