Comparative effects of UVA and UVB irradiation on the immune system of fish

Aquatic organisms can be harmed by the current levels of solar ultraviolet radiation. We have recently shown that exposure of fish to UVB irradiation alters the functioning of the fish immune system, but the effects of UVA radiation are unknown. The present study continues this work by characterizing UVA irradiation-induced immunological changes in fish. Roach, a cyprinid fish, were exposed to a single dose of either UVA (3.6 J/cm2) or UVB (0.5 J/cm2) irradiation. Both irradiations suppressed transiently mitogen-stimulated proliferation of blood lymphocytes. UVA, but not UVB, decreased hematocrit, plasma protein, and plasma immunoglobulin levels and increased the proportions of blood cells classified as unidentified leukocytes, possibly consisting of UVA-damaged lymphocytes. UVB, but not UVA, altered the functioning of head kidney and blood phagocytes, induced granulocytosis and lymphocytopenia in the blood and increased plasma cortisol concentration. These results imply that both UVA and UVB are potent modulators of the immune defence of fish.     

Ultraviolet B irradiation affects resistance of rainbow trout (Oncorhynchus mykiss) against bacterium Yersinia ruckeri and trematode Diplostomum spathaceum

Ultraviolet B (UVB) radiation is known to have various effects on the immune system of fish, but the effect on the actual disease resistance has remained largely unknown. Here we studied the effect of UVB on the resistance of rainbow trout (Oncorhynchus mykiss) against a bacterium Yersinia ruckeri, the causative agent of enteric red mouth disease, and a trematode parasite Diplostomum spathaceum, which causes cataracts in fish. The fish were exposed to UVB irradiation seven times in 14 days, and inoculated intraperitoneally with Y. ruckeri on day 5 after the first irradiation. On day 2 postinfection (p.i.), the number of viable bacteria in the kidney was lower in UVB-exposed than in unexposed fish. However, on day 8 p.i., UVB-irradiated fish had not been able to clear remaining Y. ruckeri effectively, and had a slightly higher bacterial load than controls. A similar, although not significant, effect was seen in the bacterial numbers in spleen. In the other experiment, fish were exposed to UVB for six consecutive days and then exposed to D. spathaceum. A significantly higher number of parasites was detected in the eyes of irradiated fish, indicating reduced resistance against the pathogen. Furthermore, UVB-irradiation altered the immunological and hematological parameters of fish, which also verified the immunomodulatory potential of UVB in the present study.     

Long-term UVB Irradiation Affects the Immune Functions of Carp (Cyprinus carpio) and Rainbow Trout (Oncorhynchus mykiss)

The effects of long-term, low-dose ultraviolet B (UVB) radiation on immune functions of two fish species representing different taxonomic groups, carp ( Cyprinus carpio ) and rainbow trout ( Oncorhynchus mykiss ), were assessed in this study. The fish were exposed to 7, 20 or 60 mJ cm⁻² UVB three times per week, for 6 weeks. In carp, UVB exposure affected the respiratory burst activity of blood and head kidney phagocytes, differential blood leukocyte counts and blood chemistry. Phytohemagglutinin (PHA)-stimulated in vitro proliferation responses of blood and head kidney lymphocytes, however, remained unchanged. Rainbow trout tolerated the irradiations with fewer alterations, but significant changes were detected in blood chemistry and hematocrits of the irradiated fish. These results indicate that long-term exposure to low doses of UVB induces immunomodulation in fish, and that there are species-specific differences in sensitivity to irradiation.     

Ultraviolet B irradiation modulates the immune system of fish (Rutilus rutilus, Cyprinidae). Part III: Lymphocytes

The effects of short-term exposure to ultraviolet B (UVB) radiation on lymphocyte-related parameters were studied under controlled laboratory conditions using roach (Rutilus rutilus), a cyprinid teleost, as the model fish. In vitro lymphoproliferative responses stimulated with a T-cell-specific mitogen, concanavalin A (ConA), or a B-cell-specific activator, lipopolysaccharide (LPS), were decreased in exposed fish. Also nonstimulated proliferation was lower than in unexposed fish. ConA-activated responses returned to normal levels within 7 days after exposure, but LPS-activated responses were reduced throughout the 14 day follow-up. The capability of UVB-exposed fish to produce an antibody response was studied by intraperitoneal immunization with bovine gamma-globulin (BGG). The concentration of anti-BGG antibodies in plasma as well as the number of anti-BGG-specific antibody-secreting cells in the spleen or blood were not decreased in fish exposed either to a single dose of UVB prior to immunization, or to single dose of UVB prior to immunization followed by three additional doses after immunization. Immunoglobulin M (IgM) production, when assayed as plasma IgM level or as the number of IgM-secreting cells in the spleen or blood, was not suppressed after exposure to UVB irradiation. These results indicate that a single dose of UVB or short-term exposure to UVB irradiation has no negative effects on IgM production or reactivity against antigen administered via the intraperitoneal route. However, the suppression of in vitro lymphoproliferative responses suggest that exposure to UVB has the potential to interfere with lymphocyte-related functions in fish.     

Effects of short- and long-term ultraviolet B irradiation on the immune system of the common carp (Cyprinus carpio)

Carp (Cyprinus carpio) were repeatedly exposed to 0, 60, 120 and 240 mJ/cm2 ultraviolet B (UVB) radiation three times in 1 week (short-term exposure) or 12 times in 4 weeks (long-term exposure). The effect of UVB on the functioning of the carp immune system was studied on day 2 after the final irradiation. After short-term UVB exposure, the whole-blood respiratory burst and cytotoxic activity were markedly enhanced, with parallel responses in both the number of circulating granulocytes and in the plasma cortisol concentration of the fish. These changes were not detectable after long-term exposure. The respiratory burst by head kidney granulocytes was suppressed dose dependently after both exposures, but cytotoxic activity was not affected. Exposure to UVB also modulated lymphocyte functions: nonstimulated and PHA-stimulated proliferation of head kidney lymphocytes in vitro was enhanced by both short-term and long-term exposure. LPS-stimulated proliferation was not affected by exposure nor was the number of immunoglobulin-secreting cells in the head kidney. In long-term exposure, the highest dose reduced the level of plasma IgM. This study indicates that UVB irradiation induces immunomodulation in the blood and head kidney of the carp and that the effects of short- and long-term exposure differ from each other. The results emphasize the potentially harmful impact of increased solar UVB radiation on fish immune functions.     

Ultraviolet B Irradiation Modulates the Immune System of Fish (Rutilus rutilus, Cyprinidae). I. Phagocytes

Roach ( Rutilus rutilus ) were irradiated with a single dose of ultraviolet B (UVB) radiation (0.4 J/cm²) in order to study the effects of UVB on the nonspecific immune defense mechanisms of fish. Neutrophils and macrophages were isolated from the head kidney of fish on days 1–14 postirradiation. Both random and directed migration of neutrophils, studied by migration under agarose assay, were suppressed on day 1 after UVB irradiation. The respiratory burst of phorbol 12-myristate 13-acetatestimulated neutrophils and macrophages was also suppressed at days 1 and 2 after UVB irradiation. The suppression of migration and respiratory burst were restored or the responses were even enhanced later, but on the other hand spontaneous cytotoxicity of neutrophils toward ⁵¹chromium-labeled K562 target cells stayed suppressed throughout the 14 day follow-up. This study indicates that UVB radiation has the potential to suppress the functioning of phagocytes and to compromise the immune system of fish.     

Decrease in langerhans cells and increase in lymph node dendritic cells following chronic exposure of mice to suberythemal doses of solar simulated radiation

Exposure of certain strains of mice to ultraviolet radiation (UVR) causes suppression of some innate and adaptive immune responses. One such consequence of acute UVB exposure is a reduction in the number of Langerhans cells (LC) in the epidermis and an increase in dendritic cells (DC) in lymph nodes draining the irradiated skin sites. Exposure to chronic UVB irradiation also has effects on the immune system, but it is unknown what effects are caused by repeated doses of solar simulated radiation (SSR). Consequently, the main aims of the present study were to determine whether repeated exposure to low doses of SSR would lead to similar changes in these cell populations and whether chronic doses of SSR activate a protective photoadaptation mechanism. Groups of C3H/HeN mice were irradiated daily with 3.7 J/cm(2) SSR from Cleo Natural lamps for 2, 10, 20, 30 or 60 days. Further groups of mice received an additional dose of 7.4 J/cm(2) SSR on days 2, 10, 30 or 60 to test for photoadaptation. The numbers of LC in the epidermis and DC in the lymph nodes draining irradiated skin sites were counted 24 h after the final irradiation. With the exception of mice irradiated for only 2 days, LC were significantly reduced throughout the chronic irradiation protocol, and no recovery occurred. DC numbers were significantly increased in the draining lymph nodes of mice irradiated for 20 days and 60 days.     

Salt water bathing prior to UVB irradiation leads to a decrease of the minimal erythema dose and an increased erythema index without affecting skin pigmentation

The combination of salt water baths and solar radiation is known as an effective treatment for patients with psoriasis and atopic dermatitis. To determine whether increased susceptibility to UVB radiation may contribute to this therapeutic effect we have studied the effect of bathing the skin in salt water prior to UVB irradiation. Twelve subjects were phototested on the volar aspects of their forearms with increasing doses of UVB radiation. One forearm was exposed to 5% salt water prior to irradiation. The minimal erythema dose (MED) was determined and the erythema index and skin pigmentation were assessed by photometric measurement. The combination of salt water bath and irradiation yielded a significant decrease of the MED when compared to UVB alone (median 90 mJ/cm2 vs 130 mJ/cm2, P < 0.01). Analysis of variance showed a significant influence of salt water bath on erythema (P < 0.05) but not on skin pigmentation. Within the MED test area the erythema index of the salt water exposed forearms was elevated significantly (P < 0.05) while skin pigmentation was not affected. Thus, bathing the skin in salt water leads to a decreased threshold level for the elicitation of UVB-induced erythema and a selective increase of the erythemal response. This sensitization to the effects of shortwave UVB radiation may increase immunosuppressive effects of UVB radiation and may lead to an increased efficacy of UVB phototherapy. However, there is also an increased sunburn risk when salt water baths are followed by exposure to UV radiation.     

An animal model of solar-aged skin: histological, physical, and visible changes in UV-irradiated hairless mouse skin

Albino hairless mice (Skh:HR-l) exposed to sub-erythemal doses of UVB or UVA radiation display physical, visible, and histological alterations. Skin surface replicas, transepidermal water loss, and skin fold thickness were found to change with irradiation. Visibly, the skin wrinkled with UVB and sagged with UVA exposure. These changes were graded on 3-point scales. Histological alterations included tissue thickening, loss of elastic fibers, elastosis, loss of collagen, and increases in muco-substances. The UVB alterations occur to a much lesser extent with an SPF-15 (7% PABA and 3% oxybenzone) sunscreen product. This sunscreen product had little effect on development of UVA-induced changes. However, an efficient UVA sunscreen (Parsol 1789) did reduce the UVA-induced changes. Many of the UVB-induced alterations regressed after UVB irradiation was stopped. No regression in UVA-induced alterations was observed when UVA irradiation was stopped. Qualitatively, the effects with UVA irradiation were like those observed in mouse chronological aging. These models and the convenient physical and visible grading methods described can be used to determine the effectiveness of topical treatments, such as sunscreens.     

Cell Cycle Kinetics Following UVA Irradiation in Comparison to UVB and UVC Irradiation

Abstract— There is limited information about the carcinogenic effect of longwave ultraviolet radiation (UVA: 315-400 nm). In particular very little is known about the relevant genotoxic damage caused by physiological doses of UVA radiation. A general response of cells to DNA damage is a delay or arrest of the cell cycle. Conversely, such cellular responses after UVA irradiation would indicate significant genotoxic damage. The aim of this study is to compare cell cycle kinetics of human fibroblasts after UVC (190-280 nm radiation), UVB (280-315 nm radiation) and UVA irradiation. Changes in the cell cycle kinetics were assessed by bivariate flow cytometric analysis of DNA synthesis and of DNA content. After UVC, UVB or UVA irradiation of human fibroblasts a suppression was seen of bromodeoxyuridine (BrdU) incorporation at all stages of S phase. The magnitude of this suppression appeared dose dependent. Maximum suppression was reached at 5-7 h after UVB exposure and directly after UVA exposure, and normal levels were reached 25 h after UVB and 7 h after UVA exposure. The lowered BrdU uptake corresponded with a lengthening of the S phase. No dramatic changes in percentages of cells in G₁, S and G₂/M were seen after the various UV irradiations. Apparently, UVA irradiation, like UVB and UVC irradiation, can temporarily inhibit DNA synthesis, which is indicative of genotoxic damage.     

N-acetyl-L-cysteine prevents DNA damage induced by UVA, UVB and visible radiation in human fibroblasts

The thiol N-acetyl-L-cysteine (NAC) is a source of cysteine for the synthesis of the endogenous antioxidant glutathione (GSH) which is depleted by ultraviolet radiation. It is also associated with the scavenging of reactive oxygen species (ROS). In this study the effects of NAC were examined in cultured human fibroblasts during prolonged exposure to ultraviolet B (UVB), ultraviolet A (UVA) and visible irradiation (280-700 nm), delivered by a 150 W xenon-arc lamp. The alkaline comet assay was used to assess the DNA damage in individual cells. It was found that incubating skin and lung fibroblasts at 37 degrees C for 1 h with an optimal 6 mM NAC supplement prior to light exposure, significantly reduced the level of DNA damage in both cell types, however, the skin fibroblasts were less sensitive to xenon-arc lamp irradiation than lung fibroblasts. NAC incubation resulted in an initial delay in DNA damage when the cells were irradiated. There was also a significant reduction in the overall levels of DNA damage observed with continued irradiation. NAC significantly reduced the DNA damage produced in lung fibroblasts depleted of normal GSH protection by the glutamylcysteinyl synthetase inhibitor, L-buthionine-[S,R]-sulfoximine. Although the specific mechanism of NAC protection has not yet been elucidated, these results support the hypothesis that NAC may protect the cells directly, by scavenging ROS induced by UVA and visible radiation, and indirectly by donating cysteine for GSH synthesis.     

Action Spectra for UVB Impacts on Blepharisma japonicum Motility and Photobehavior

Abstract— The ciliate Blepharisma japonicum was exposed to artificial polychromatic and monochromatic UV radiation to evaluate the relative roles of UVB (280–315 nm UV radiation) and UVA (315–400 nm UV radiation) in altering its motility and photobehavior and to determine absolute weighting coefficients for these effects in the UVB range. Under polychromatic UV irradiation B. japonicum cells showed a severe reduction of cell speed and of the capability to respond to light stimuli. At low doses, however, UV caused a significant increase in the average velocity of a cell population. The UVB exclusion experiments indicated that UVA does not significantly alter motility and photoresponsiveness. The increase and the subsequent decrease in cell velocity was observed also under monochromatic irradiation at 281, 290 and 300 nm, whereas at 310 nm cells swim faster up to the highest photon flux density used. The cell capability of reacting to photic stimuli, conversely, steadily declined with increasing photon flux density at all the tested UVB wavelengths. The action spectra for the alteration of cell velocity and the impairment of photoresponsiveness show that the lower the irradiation wavelength, the more remarkable are the UVB effects and suggest different targets for the increase and the decrease in cell velocity.     

Plantamajoside Inhibits UVB and Advanced Glycation End Products‐Induced MMP‐1 Expression by Suppressing the MAPK and NF‐κB Pathways in HaCaT Cells

Photoaging and glycation stress are major causes of skin deterioration. Oxidative stress caused by ultraviolet B (UVB) irradiation can upregulate matrix metalloprotease 1 (MMP‐1), a major enzyme responsible for collagen damage in the skin. Advanced glycation end products (AGEs) accumulate via gradual formation from skin proteins, especially from long‐lived proteins such as dermal elastin and collagen. Plantamajoside (PM), isolated from Plantago asiatica, has various biological effects including anti‐inflammatory and antioxidant effects. In this study, we assessed the protective effects of PM on a human keratinocyte cell line (HaCaT) and primary human dermal fibroblasts (HDF) against stress caused by glyceraldehyde‐induced AGEs (glycer‐AGEs) with UVB irradiation. We found that PM attenuated UVB‐ and‐glycer‐AGEs‐induced MMP‐1 expression in HaCaT and HDF cells and proinflammatory cytokines expression by inhibiting the phosphorylation of mitogen‐activated protein kinases (MAPKs) activated by reactive oxygen species. Specific inhibitors of NF‐κB and MAPKs attenuated the induced expression of MMP‐1. PM also inhibited the phosphorylation of IκBα, and reduced nuclear translocation of NF‐κB in these cells. Furthermore, PM attenuated the upregulation of receptor for AGEs (RAGE) by glycer‐AGEs with UVB irradiation. Therefore, our findings strongly suggest that PM is a promising inhibitor of skin photoaging.     

Effects of ultraviolet B on epidermal morphology, shedding, lipid peroxide, and antioxidant enzymes in Cope's rat snake (Elaphe taeniura)

Cope's rat snakes (Elaphe taeniura) favor to expose under sunlight in order to increase their body temperature simultaneously increasing the risk of skin damage by ultraviolet B (UVB) irradiation. We have investigated the effects of UVB irradiation on their skin. Results show that the UVB transmission of the keratinous layer was only 5.1+/-0.36%. The peak of epidermal damage and malondialdehyde (MDA) content, a product of lipid peroxidation, simultaneously occurred 72-96, 48 or 24 h after exposure to 300, 500 and 800 mJ/cm2 of UVB radiation, respectively. Superoxide dismutase (SOD) activity was inhibited by UVB and the lowest activity occurred 24, 48, 12 and 12 h after exposure to 110, 300, 500 and 800 mJ/cm2 of UVB, respectively. SOD activity recovered later to some extent but mostly remained below control level. After exposure to different doses of UVB radiation, catalase (CAT) activity was inhibited immediately, and then gradually recovered and even increased to peak levels above control level. The highest CAT levels accompanied the most serious damage of skin morphology. Later on, CAT activity decreased and recovered again close to or below control level, which was accompanied by shedding off the damaged epidermal complex. This indicated that the epidermal damage induced by UVB is closely related to lipid peroxidation, where CAT acts as a primary antioxidant enzyme. Moreover, the keratinous layer protects the viable cell layer against UVB damage as well.     

Dendrobium nobile Lindl Polysaccharides Attenuate UVB-induced Photodamage by Regulating Oxidative Stress,Inflammation and MMPs Expression in Mice Model

Acute ultraviolet B (UVB) irradiation predominantly leads to various skin disorders caused by photodamage. The major causes of UVB-induced photodamage include oxidative stress, inflammatory infiltration and collagen degradation. The aim of the study was to elucidate whether DNP had protective effect on the skin of KM mice when exposed to UVB irradiation. The DNP protective properties to skin appearance and histopathological alterations in KM mice were evaluated by hematoxylin–eosin staining, toluidine blue staining, Gomori staining and Masson's trichrome staining and mast cell staining. In this study, DNP pretreatment promoted the activities of antioxidant enzymes, including superoxide dismutase, catalase and glutathione peroxidase, while decreased malondialdehyde level in UVB-irradiated skin, along with downregulation of proteins expression of matrix metalloproteinases and reduction in the level of the proinflammatory cytokines. Based on these findings, we demonstrated that DNP displayed strong ameliorative effects on UVB-induced acute photodamage for the first time, indicating that it would be a promoting ingredient candidate that could be used in antiphotodamage.     

Cell Cycle Effects and Concomitant p53 Expression in Hairless Murine Skin after Longwave UVA (365 nm) Irradiation: A Comparison with UVB Irradiation

Abstract— Ultraviolet A (UVA,315–400 nm) radiation is known to be a complete carcinogen, but in contrast to UVB (280-315 nm) radiation, much of the cell damage is oxygen dependent (mediated through reactive oxygen species), and the dominant premutational DNA lesion(s) remains to be identified. To investigate further the basic differences in UVA and UVB carcinogenesis, we compared in vivo cellular responses, viz. cell cycle progression and transient p53 expression in the epidermis, after UVA1 (340-400 nm) exposure with those after broadband UVB exposure of hairless mice. Using flow cytometry we found a temporary suppression of bromodeoxyuridine (BrdU) uptake in S-phase cells both after UVB and UVA1 irradiation, which only in the case of UVB is followed by an increase to well over control levels. With equally erythemogenic doses (1-2 MED), the modulation of BrdU uptake was more profound after UVB than after UVA1 irradiation. Also, a marked transient increase in the percentage of S-phase cells occurred both after UVB and after UVA1 irradiation, but this increase evolved more rapidly after UVA1 irradiation. Further, p53 expression increased both after UVB and UVA1 irradiations, with peak expression already occurring from 12 to 24 h after UVA1 exposure and around 24 h after UVB exposure. Overall, UVA1 radiation appears to have less of an impact on the cell cycle than UVB radiation, as measured by the magnitude and duration of changes in DNA synthesis and cells in S phase. These differences are likely to reflect basic differences between UVB and UVA1 in genotoxicity and carcinogenic action.     

Effect of cyclobutane pyrimidine dimers on apoptosis induced by different wavelengths of UV.

Ultraviolet radiation within three different wavelength ranges, UVA (340-400 nm), UVB (290-320 nm) or UVC (200-290 nm), was shown to induce apoptosis in OCP13 cells, derived from the medaka fish. Morphological changes such as cell shrinkage and a decrease in the number of nucleoli appeared 4 h after UVA, UVB or UVC irradiation, although with different relative efficiencies. Doses required to induce apoptosis with similar efficiencies were about 2500-fold higher for UVA and 10-fold higher for UVB than for UVC. The following phenomena occurred after UVA irradiation but not after UVB or UVC irradiation. (1) Ultraviolet-A-induced cell detachment occurred with or without cycloheximide pretreatment. (2) Cells attached to plastic showed morphological changes such as rounding up of nuclei without a change in the cell distribution. (3) Morphological changes after UVA irradiation could not be evaded by photorepair treatment. (4) Morphological changes did not occur in cells attached to glass coverslips but only those in plastic dishes. (5) Apoptosis occurred without detectable increase of caspase-3-like activity. (6) Morphological changes were inhibited by N-acetylcysteine, a scavenger of active oxygen species. These results suggest the existence of two different pathways leading to apoptosis, one for long- (UVA) and the other for short- (UVB or UVC) wavelength radiation.     

Histopathological Analysis of UVB and IR Interaction in Rat Skin

To determine the chronic skin effects caused by the interaction of infrared and ultraviolet B radiations, male Rattus norvegicus (Wistar) (2 months old) were exposed for 15 days to infrared radiation (600–1500 nm, with a peak at 1000 nm, n = 12) for 30 min (1080 J cm^?2) (IRo); to ultraviolet B radiation (peak emission at 313 nm, n = 9) for 90 min (55.08 J cm^?2) (UVB); to infrared radiation followed after 90 min by ultraviolet B (n = 6) (IRUVB) and to ultraviolet B followed after 90 min by infrared radiation (n = 9) (UVBIR). Skin samples were collected and histopathological analysis showed the presence of acanthosis, parakeratotic and orthokeratotic hyperkeratosis, intraepidermal pustules, keratin pearls, detachment of epidermis, collagen necrosis, inflammatory infiltrate, vasodilation, basal cell vacuolization and superficial dermis degeneration both in UVB and UVBIR treatments. IRUVB animals showed the same characteristics as above except for parakeratotic hyperkeratosis, keratin pearls and superficial dermis degeneration. To conclude, infrared radiation exposure after ultraviolet B irradiation increases skin damage without protecting the tissue, while infrared radiation exposure before ultraviolet B irradiation showed a protective effect against ultraviolet skin damage.     

REASSESSMENT OF THE DIFFERENTIAL EFFECTS OF ULTRAVIOLET AND IONIZING RADIATION ON HIV PROMOTER: THE USE OF CELL SURVIVAL AS THE BASIS FOR COMPARISONS

Abstract: Effects of different radiation treatments on the human immunodeficiency virus-1 (HIV) promoter were reassessed for exposures comparable to those encountered in clinical or cosmetic practice, using survival of the host cell as a basis for comparisons. The exposures were performed with two ultraviolet radiation sources commonly used as medical or cosmetic devices (UVASUN 2000 and FS20 lamps), a germicidal (G15T8) lamp and an X-ray machine. The UVC component of the FS20 lamp was filtered out. The emission spectra of the lamps were determined. The characteristics of these sources allowed us to discriminate among effects of UVA1 (340–400 nm), UVB + UVA2 (280–340 nm) and UVC (254 nm) radiations. Effects of irradiation were ascertained using cultures of HeLa cells stably transfected with the HIV promoter linked to a reporter—chloramphenicol acetyl transferase—gene. The exposures used caused at least two logs of cell killing. In this cytotoxicity range, UVA1 or X radiations had no effect on the HIV promoter, whereas UVB + UVA2 or UVC radiations activated the HIV promoter in a fluence-dependent manner. Survivals following exposure to UVB + UVA2 or UVC radiation were (1) at the lowest measurable HIV promoter activation, 30 and 20%, respectively, (2) at one-half maximal activation, 6 and 3%, respectively and (3) at the maximal activation, 0.5 and 0.2%, respectively. The results suggest that, among the radiations studied, UVB is the most important modality from the viewpoint of its potential effects on HIV-infected individuals, since (1) UVA1 or X radiations have no effects on the HIV promoter, (2) human exposure to UVC radiation is infrequent and (3) human UVB exposure is very common.