Human cytomegalovirus UL76 induces chromosome aberrationsReport as inadecuate

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Journal of Biomedical Science

, 16:107

First Online: 25 November 2009Received: 15 April 2009Accepted: 25 November 2009DOI: 10.1186-1423-0127-16-107

Cite this article as: Siew, VK., Duh, CY. & Wang, SK. J Biomed Sci 2009 16: 107. doi:10.1186-1423-0127-16-107


BackgroundHuman cytomegalovirus HCMV is known to induce chromosome aberrations in infected cells, which can lead to congenital abnormalities in infected fetuses. HCMV UL76 belongs to a conserved protein family from herpesviruses. Some reported roles among UL76 family members include involvement in virulence determination, lytic replication, reactivation of latent virus, modulation of gene expression, induction of apoptosis, and perturbation of cell cycle progression, as well as potential nuclease activity. Previously, we have shown that stable expression of UL76 inhibits HCMV replication in glioblastoma cells.

MethodsTo examine chromosomal integrity and the DNA damage signal γ-H2AX in cells constitutively expressing UL76, immunofluorescent cell staining and Western blotting were performed. The comet assay was employed to assess DNA breaks in cells transiently expressing UL76.

ResultsWe report that stably transfected cells expressing UL76 developed chromosome aberrations including micronuclei and misaligned chromosomes, lagging and bridging. In mitotic cells expressing UL76, aberrant spindles were increased compared to control cells. However, cells with supernumerary centrosomes were marginally increased in UL76-expressing cells relative to control cells. We further demonstrated that UL76-expressing cells activated the DNA damage signal γ-H2AX and caused foci formation in nuclei. In addition, the number of cells with DNA breaks increased in proportion to UL76 protein levels.

ConclusionOur findings suggest that the virus-associated protein UL76 induces DNA damage and the accumulation of chromosome aberrations.

Electronic supplementary materialThe online version of this article doi:10.1186-1423-0127-16-107 contains supplementary material, which is available to authorized users.

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Author: Voon-Kwan Siew - Chang-Yih Duh - Shang-Kwei Wang


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