THE EFFECT OF UV-B IRRADIATION ON SECONDARY EPIDERMAL INFECTION OF MICE WITH HERPES-SIMPLEX VIRUS TYPE-1

Citation
Aa. Elghorr et M. Norval, THE EFFECT OF UV-B IRRADIATION ON SECONDARY EPIDERMAL INFECTION OF MICE WITH HERPES-SIMPLEX VIRUS TYPE-1, Journal of General Virology, 77, 1996, pp. 485-491
Citations number
32
Categorie Soggetti
Virology,"Biothechnology & Applied Migrobiology
Journal title
ISSN journal
00221317
Volume
77
Year of publication
1996
Part
3
Pages
485 - 491
Database
ISI
SICI code
0022-1317(1996)77:<485:TEOUIO>2.0.ZU;2-E
Abstract
Previous studies have indicated that suberythemal ultraviolet B (UV-B) irradiation of C3H mice before primary infection with herpes simplex virus (HSV) type 1 does not result in increased morbidity or mortality , but a suppressed delayed type hypersensitivity (DH) to the virus can be demonstrated. Any effect of UV radiation on pathogenesis during se condary epidermal HSV infection has not been previously examined. Mice were immunized by subcutaneous injection of inactivated HSV and, 5 da ys later, one group was UV-B-irradiated. The next day all mice were ch allenged epidermally with HSV. Most of the mice (92%) in the irradiate d group developed severe lesions, whilst 59% of the nonirradiated grou p had mild lesions and 30% no lesions. Infectious virus was not isolat ed from the adrenal glands after challenge in either group. In additio n, the DH to the virus was not affected by the UV exposure. The number s of lymphocytes and dendritic cells in the lymph nodes draining the s ite of epidermal infection were increased in the UV group compared wit h the nonirradiated group. Following challenge, the percentage of CD4( +) and CD8(+) lymphocytes in lymph nodes was unaltered but the MHC cla ss II expression on dendritic cells in these lymph nodes was reduced b y UV exposure. The lymphoproliferative response in vitro of lymph node cells revealed a suppressed response to HSV and to the mitogen concan avalin A in the irradiated group. Thus, UV irradiation prior to epider mal secondary infection with HSV led to more severe infections due, pe rhaps, to a modulation in local antigen presentation.