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Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
Published on: September 28, 2022
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Epstein-Barr virus particles induce centrosome amplification and chromosomal instability
Anatoliy Shumilov1,2,3, Ming-Han Tsai1,2,3, Yvonne T Schlosser4
1German Cancer Research Centre (DKFZ), Unit F100, 69120 Heidelberg, Germany.
Nature Communications
|February 11, 2017
Summary
Epstein-Barr virus (EBV) infection increases centrosome amplification in B-lymphocytes, leading to chromosomal instability. This occurs even without chronic infection, mediated by viral protein BNRF1, increasing cancer risk.
Area of Science:
- Virology
- Cancer Biology
- Cell Biology
Background:
- Epstein-Barr virus (EBV) is linked to cancer development.
- EBV lytic replication is a known risk factor for certain cancers.
Purpose of the Study:
- To investigate the mechanism by which EBV contributes to cancer development.
- To determine if EBV infection causes chromosomal instability.
Main Methods:
- In vitro and mouse models of EBV infection in B-lymphocytes.
- Analysis of centrosome amplification and chromosomal instability.
- Use of virus-like particles (VLPs) with and without EBV DNA.
- Investigation of the role of viral protein BNRF1.
Main Results:
- EBV infection of B-lymphocytes increases centrosome amplification and chromosomal instability.
- This effect is mediated by EBV particles, not solely by chronic infection.
- Viral protein BNRF1 is identified as a key inducer of centrosome amplification.
- BNRF1-deficient viruses show reduced capacity to induce this effect.
Conclusions:
- EBV particles can induce chromosomal instability through centrosome amplification without establishing chronic infection.
- This mechanism contributes to cancer development in tumors that may not harbor the viral genome.
- Identifies a novel pathway linking EBV to oncogenesis.
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