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The combined effects of irradiation and herpes simplex virus type 1 infection on an immortal gingival cell line

Aaro Turunen1*, Veijo Hukkanen2, Michaela Nygårdas2, Jarmo Kulmala3 and Stina Syrjänen1

Author Affiliations

1 Institute of Dentistry, Department of Oral Pathology, University of Turku, Lemminkäisenkatu 2, 20520 Turku, Finland

2 Department of Virology, University of Turku, Kiinanmyllynkatu 13, 20520 Turku, Finland

3 Department of Radiotherapy, Turku University Hospital, Clinic of Oncology, Hämeentie 11, 20521 Turku, Finland

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Virology Journal 2014, 11:125  doi:10.1186/1743-422X-11-125

Published: 8 July 2014



Oral mucosa is frequently exposed to Herpes simplex virus type 1 (HSV-1) infection and irradiation due to dental radiography. During radiotherapy for oral cancer, the surrounding clinically normal tissues are also irradiated. This prompted us to study the effects of HSV-1 infection and irradiation on viability and apoptosis of oral epithelial cells.


Immortal gingival keratinocyte (HMK) cells were infected with HSV-1 at a low multiplicity of infection (MOI) and irradiated with 2 Gy 24 hours post infection. The cells were then harvested at 24, 72 and 144 hours post irradiation for viability assays and qRT-PCR analyses for the apoptosis-related genes caspases 3, 8, and 9, bcl-2, NFκB1, and viral gene VP16. Mann–Whitney U-test was used for statistical calculations.


Irradiation improved the cell viability at 144 hours post irradiation (P = 0.05), which was further improved by HSV-1 infection at MOI of 0.00001 (P = 0.05). Simultaneously, the combined effects of infection at MOI of 0.0001 and irradiation resulted in upregulation in NFκB1 (P = 0.05). The combined effects of irradiation and HSV infection also significantly downregulated the expression of caspases 3, 8, and 9 at 144 hours (P = 0.05) whereas caspase 3 and 8 significantly upregulated in non-irradiated, HSV-infected cells as compared to uninfected controls (P = 0.05). Infection with 0.0001 MOI downregulated bcl-2 in non-irradiated cells but was upregulated by 27% after irradiation when compared to non-irradiated infected cells (P = 0.05). Irradiation had no effect on HSV-1 shedding or HSV gene expression at 144 hours.


HSV-1 infection may improve the viability of immortal cells after irradiation. The effect might be related to inhibition of apoptosis.

HSV-1; Herpesviruses; Irradiation; Oral cancer; Apoptosis; Immortal gingival cells; Radiation treatment