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Measles virus-induced modulation of host-cell gene expression
Gert Bolt1, Kurt Berg2, Merete Blixenkrone-Møller1
1Laboratory of Virology and Immunology, Royal Veterinary and Agricultural University, Bülowsvej 17, 1870 Frederiksberg C, Denmark1.
The Journal of General Virology
|April 19, 2002
Summary
Measles virus (MV) infection alters gene expression in human immune cells. MV upregulates 17 genes, including those involved in apoptosis and the interferon system, potentially impacting measles pathogenesis.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Measles virus (MV) infection impacts host cell gene expression.
- Understanding these changes is crucial for elucidating measles pathogenesis.
Purpose of the Study:
- To investigate the influence of measles virus infection on gene expression in human peripheral blood mononuclear cells (PBMCs).
- To identify specific host genes upregulated by MV infection and confirm their activation at the protein level.
Main Methods:
- Utilized cDNA microarrays to compare mRNA levels of over 3000 genes between uninfected and MV-infected PBMCs.
- Employed Reverse Transcription Polymerase Chain Reaction (RT-PCR) to validate microarray findings.
- Analyzed protein level changes for selected upregulated genes.
Main Results:
- MV infection upregulated a total of 17 host cell genes.
- The Edmonston MV strain demonstrated more efficient growth and stronger induction of host gene upregulation compared to the wild-type MV.
- Upregulated genes included those involved in the anti-apoptotic B cell lymphoma 3 (Bcl-3) pathway, NF-kappaB p52 subunit, interferon system (e.g., interferon regulatory factor 7), and endoplasmic reticulum stress response (e.g., CHOP/GADD153).
Conclusions:
- Measles virus infection activates specific cellular mechanisms and pathways in PBMCs.
- These activated pathways, including those related to apoptosis and stress response, may contribute to the pathogenesis of measles.
- The findings highlight the complex interplay between MV and host cell gene regulation.