Ultraviolet radiation (UVR) suppresses many aspects of cell-mediated immunity but it is uncertain whether solar UV exposure alters resistance to human infectious diseases. Varicella-zoster virus (VZV) causes varicella (chickenpox) and can reactivate from latency to cause zoster (shingles). The monthly incidence of chickenpox and zoster in a defined Polish population over 2 years was recorded and ground level solar UV was measured daily. There was a significant seasonality of UVR. Evidence of seasonal variation was found for all zoster cases and for zoster in males, with the lowest number of cases in the winter. The number of zoster cases with lesions occurring on exposed body sites (the face) demonstrated highly significant seasonality with a peak in July/August. Seasonal models for UVR and zoster cases showed similar temporal patterns. By contrast, for varicella, the maximum number of cases was found in March and the minimum in August/September, probably explained by the respiratory spread of VZV. It is tempting to speculate that the increase in solar UVR in the summer could induce suppression of cellular immunity, thus contributing to the corresponding rise in the incidence of zoster.

BCC is a very complex disease, with many factors influencing its development. Environmental factors are very important for the prevalence of BCC, and most of them can be avoided. The exposure to ultraviolet radiation is undoubtedly of great risk; therefore, the national campaigns against aggressive, seasonal sun exposure, especially in children and adolescents, as well as using sunscreens, are of great value in the fight against BCC development.

BACKGROUND: The association of allergic diseases, drug adverse reactions and elevated total immunoglobulin E (IgE) concentration in systemic lupus erythematosus patients remains controversial. The aim of the study was to investigate the prevalence of those features in active and inactive systemic lupus erythematosus patients, and in the control group as well. METHODS: Total IgE concentration was evaluated by enzyme-linked immunosorbent assay. RESULTS AND CONCLUSIONS: The results of our study revealed that concomitant allergic diseases were not more frequent in systemic lupus erythematosus patients than in the general population. Total IgE concentration was significantly higher during the active stage of the disease. Drug reactions were very frequent but not connected with IgE elevation. Our results indicate that IgE may play a role in lupus pathogenesis, especially in the active phase of the disease.

SUMMARYVaricella zoster virus (VZV) causes varicella (chickenpox) as the primary infection and zoster (shingles) on reactivation from latency, often many years later. One of the most common and most severe sequela of zoster is postherpetic neuralgia (PHN). Apart from age, factors which predispose towards PHN are unknown. In the present study, the concentration of a variety of Th1 and Th2 cytokines in the serum of 30 zoster patients at the time of the acute disease were correlated with the subsequent development of PHN in nine of these patients, but no association was found. In addition, although some cytokines such as IFN-g , IL-6 and IL-8 were slightly raised in the zoster group compared with a group of normal healthy subjects of a similar age distribution, these differences only verged on significance. Antibody titres to VZV were raised in the zoster group compared with the controls but these did not differ between the patients who developed PHN and those who did not. Biopsies of zoster lesions were collected from nine patients. There were significantly fewer infiltrating lymphocytes in the lesions of the three patients who subsequently developed PHN compared with the six who did not, although the expression of the neuropeptide, substance P, did not differ between the two groups. It is possible that the poor inflammatory response at the time of the acute zoster may result in less effective containment of the VZV and more damage in the dermatome, thus contributing to the persistence of the neuralgia.

No abstract

No abstract

No abstract

SUMMARYHerpes simplex virus (HSV) is known to possess several mechanisms whereby it can evade the normal host immune defences. In this study the expression of the immunosuppressive cytokine, interleukin (IL)-10, was monitored following infection of a murine keratinocyte cell line (PAM-212) and compared with the expression of two proin¯ammatory cytokines: IL-1a and tumour necrosis factor (TNF)-a. The PAM-212 cells were infected at a multiplicity of 0 . 5 with a clinical isolate of HSV type 1, and the mRNA of the three cytokines was assessed by semiquantitative reverse transcription±polymerase chain reaction (RT±PCR) over the following 24 hr. By 12 hr postinfection the amount of IL-10 mRNA had increased signi®cantly to ®ve-fold greater than that found in uninfected cells (P<0 . 01), and this elevated level was maintained until at least 24 hr postinfection. In contrast, IL-1a and TNF-a mRNAs were not signi®cantly up-regulated by the HSV infection. Immunostaining with an IL-10 monoclonal antibody (mAb) revealed that cytoplasmic IL-10 protein had increased by 6 ±12 hr postinfection. This quantity was further increased at 24 hr postinfection, when the viral cytopathic effect was apparent. Viral replication was necessary, but not suf®cient on its own, for IL-10 induction. Experiments with HSV mutants lacking functional transactivating factors suggested that the viral transactivating proteins ICP-0 and VP-16 may be necessary for HSV-induced IL-10 expression. Thus, the up-regulation in the expression of IL-10 mRNA and protein induced by HSV early in the infection of keratinocytes represents a speci®c response and may be part of the viral strategy to avoid local immune defence mechanisms in the skin.