The effect of UV-B irradiation on secondary epidermal infection of mice with herpes simplex virus type 1

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 secondary epidermal HSV infection has not been previously examined. Mice were immunized by subcutaneous injection of inactivated HSV and, 5 days later, one group was UV-B-irradiated.The next day all mice were challenged epidermally with HSV. Most of the mice (92 %) in the irradiated group developed severe lesions, whilst 59% of the nonirradiated group had mild lesions and 30 % no lesions. Infectious virus was not isolated from the adrenal glands after challenge in either group. In addition, the DH to the virus was not affected by the UV exposure. The numbers oflymphocytes and dendritic cells in the lymph nodes draining the site of epidermal infection were increased in the UV group compared with the nonirradiated group. Following challenge, the percentage of CD4 + and CD8 + lymphocytes in lymph nodes was unaltered but the MHC class II expression on dendritic cells in these lymph nodes was reduced by UV exposure. The lymphoproliferative response in vitro of lymph node cells revealed a suppressed response to HSV and to the mitogen concanavalin A in the irradiated group. Thus, UV irradiation prior to epidermal secondary infection with HSV led to more severe infections due, perhaps, to a modulation in local antigen presentation.

Transcutaneous immunisation with herpes simplex virus stimulates immunity in mice

“…A plaque‐purified strain of HSV‐1, isolated from a clinical case and passaged four times in Vero cells at a multiplicity of infection of 0.2, was used throughout [9]. The virus was cultured and titrated as plaque forming units (PFU) on monolayers of Vero cells as previously described [10]. Inactivated HSV was prepared by UV irradiating a virus stock with 12 000 J m −2 UV‐B.…”

“…The size of the lesions that formed on the backs of the mice was then measured with a ruler in two dimensions, each day for the next 10 days. This procedure has previously been shown to mimic a natural epidermal HSV infection and result in the formation of moderate vesicular lesions on the infected skin [10].…”

The Dark and the Sunny Sides of UVR-Induced Immunosuppression: Photoimmunology Revisited

“…In fact, numerous experimental models have shown that UVR suppresses immune responses against bacterial, viral, and fungal infections (Chapman et al, 1995). For example, mice that were immunized with the herpes simplex virus developed severe ulcerated lesions upon cutaneous herpes virus inoculation during which they were exposed to UVR before inoculation (El-Ghorr and Norval, 1996).…”

Systemic suppression of human peripheral blood phagocytic leukocytes after whole-body UVB irradiation

“…In addition to locally compromising the host's defense against skin tumors, UVB-induced systemic immune suppression may influence the development and course of infectious disease. Although the evidence that this type of immune suppression occurs in humans is less compelling and still incomplete, studies with rodents have clearly demonstrated that exposure to UVB suppresses the resistance against both systemic and non-skin-associated local infections [3][4][5][6][7]. However, the mechanism by which UVB impairs the immunity to infectious disease is not known.…”