Email updates

Keep up to date with the latest news and content from Virology Journal and BioMed Central.

Open Access Research

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

For all author emails, please log on.

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