Enhancement of genetic instability in human B cells by Epstein–Barr virus latent infection

The level of genetic instability, as assessed by micronucleus (MN) formation, was higher in Epstein–Barr virus (EBV)-converted B-cell lines with one copy of the EBV genome integrated in each cell than in the parental, EBV-negative, B lymphoma cells. MN induced by EBV latency, as analysed by in situ...

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Bibliographic Details
Published in:Mutagenesis 2001-05, Vol.16 (3), p.203-208
Main Authors: Gualandi, Giampiero, Giselico, Luigi, Carloni, Manuela, Palitti, Fabrizio, Mosesso, Pasquale, Alfonsi, Alberto Maria
Format: Article
Language:English
Subjects:
Antioxidants - pharmacology
Apoptosis
B-Lymphocytes - metabolism
B-Lymphocytes - virology
Biological and medical sciences
Blotting, Southern
Cell Line
Demecolcine - pharmacology
Epstein-Barr virus
Flow Cytometry
Fundamental and applied biological sciences. Psychology
Glutathione - metabolism
Herpesvirus 4, Human - metabolism
Humans
Hydrogen Peroxide - pharmacology
In Situ Hybridization
Infection - genetics
Micronucleus Tests
Molecular and cellular biology
Molecular genetics
Mutagenesis. Repair
Mutation
Oxidative Stress
Oxygen - metabolism
Peroxides - metabolism
Time Factors
Tumor Cells, Cultured
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Summary:The level of genetic instability, as assessed by micronucleus (MN) formation, was higher in Epstein–Barr virus (EBV)-converted B-cell lines with one copy of the EBV genome integrated in each cell than in the parental, EBV-negative, B lymphoma cells. MN induced by EBV latency, as analysed by in situ hybridization, contained mainly centromeric regions, indicating that the presence of EBV affects the segregation of entire chromosomes. The instability was inhibited by treatment with antioxidants. Flow cytometric analysis indicated that there was a higher basal level of peroxides in EBV+ cells. Direct oxidative stress caused by hydrogen peroxide (which is known to be both apoptogenic and mutagenic) enhanced the number of MN only in an EBV-converted clone. These cells were also resistant to apoptosis, as expected, suggesting that in the parental EBV cells apoptosis may efficiently eliminate cells with genetic damage. These results show for the first time a direct involvement of EBV in the induction of genetic instability, suggesting that it could contribute to tumour progression.
ISSN:0267-8357
1464-3804
1464-3804
DOI:10.1093/mutage/16.3.203