UVB and PUVA therapies in HIV patients: are they safe?

Beer, Janusz Z.; Zmudzka, Barbara Z.

doi:10.1111/j.1600-0781.1997.tb00122.x

Cited by 7 publications

(6 citation statements)

References 10 publications

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“…HIV gene expression is dramatically enhanced by the exposure of HIV-infected or stably transfected HIV reporter gene cell constructs to specific chemical agents, cytokines and environmental stress, including UV and ionizing radiation, implicating these as potential activating agents of latent virus infection that may influence the course of HIV pathogenesis (1)(2)(3)(4)(5)(6)(19)(20)(21)(22). Phorbol ester and cytokines, like tumor necrosis factor-␣ (TNF-␣) and interleukin-1 (IL-1), stimulate HIV gene expression in a cell type-specific manner (23).…”

Section: Discussionmentioning

confidence: 99%

Role of the p38 and MEK-½/p42/44 MAP Kinase Pathways in the Differential Activation of Human Immunodeficiency Virus Gene Expression by Ultraviolet and Ionizing Radiation

Taher

Hershey

Oakley

et al. 2007

Photochemistry and Photobiology

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Ultraviolet (UV) radiation is a potent activator of human immunodeficiency virus (HIV) gene expression in a HeLa cell clone having stably integrated copies of an HIVcat (cat gene under control of the HIV promoter) reporter construct, whereas ionizing radiation is ineffective. UV‐activated HIV gene expression is completely blocked by the specific p38 mitogen‐activated protein (MAP) kinase inhibitor SB203580 and by expression of a kinase‐inactive p38 mutant that interferes with normal p38 function, suggesting that this stress‐activated protein kinase plays an important role in UV‐mediated transcriptional activation of HIV. In support of these findings, we show here that Western blot analysis demonstrated rapid and significant activation of p38 MAP kinase by UV. On the other hand, γ‐radiation activated p38 MAP kinase very poorly in HeLa cells at both low and high doses at times (5–30 min) when UV radiation was effective. UV radiation also activated HIV gene expression (≤9‐fold) in 1G5 Jurkat T‐cells stably transfected with a luciferase reporter gene under control of the HIV promoter. In these cells, γ‐radiation stimulated HIV gene expression but to a lesser extent (≤3‐fold) and with different kinetics than after UV radiation, and this response was obliterated by the incubation of cells with the mitogen‐activated protein kinase/Erk kinase (MEK)‐½ inhibitor PD98059. This result suggests that in these cells signaling in response to γ‐radiation is transduced through the MEK‐½/p42/44 MAP kinase pathway to increase HIV gene expression. All combined, these results suggest that activation of p38 MAP kinase is necessary for efficient HIV gene expression triggered by DNA damaging agents, and, in a cell type‐specific manner, activation of the MEK‐½/p42/44 MAP kinase pathway is important for triggering a response to γ‐radiation. Thus, it appears as if UV signaling leading to HIV gene expression requires the p38 MAP kinase pathway whereas activation by γ‐radiation requires the MEK‐½/p42/44 MAP kinase pathway.

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Section: Discussionmentioning

confidence: 99%

Role of the p38 and MEK-½/p42/44 MAP Kinase Pathways in the Differential Activation of Human Immunodeficiency Virus Gene Expression by Ultraviolet and Ionizing Radiation

Taher

Hershey

Oakley

et al. 2007

Photochemistry and Photobiology

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“…Bei der Behandlung der papulösen Dermatitis wurde die UVB-Bestrahlung zunächst 3-bis 4mal wöchentlich eingeleitet mit einer initialen Bestrahlungsdosis, die meist zwischen 0,07 und 0,1 J/cm 2 lag. Die potentiell immunsuppressive Wirkung des UV-Lichts läßt jedoch bei HIV-positiven Patienten eine negative Beeinflussung der Grundkrankheit befürchten, so daß die Lichttherapie häufig erst als Ultima ratio zur Anwendung kommt [3,5,9,22,35,37]. Im Rahmen des therapeutischen Einsatzes von UV-Strahlung spielt der Einfluß der UV-Strahlung auf das Immunsystem der Haut eine wichtige Rolle und führte zur erfolgreichen Anwendung bei der Behandlung der Mycosis fungoides, der Dermatitis atopica, der Psoriasis und einer Reihe anderer Dermatosen [1,6,10,39].…”

Section: Uv-therapie Bei Hiv-patientenunclassified

“…Ring et al fanden unter HIV-negativen Homosexuellen doppelt so viele Atopiker wie unter HIV-positiven Homosexuellen [30]. die Zahl HIV-infizierter Zellen in der Haut relativ gering [3]. Später wiesen Zmudzka u.…”

Section: Besprechungunclassified

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UV-Therapie bei HIV-Patienten

Schoppelrey¹,

Breit²

1999

Der Hautarzt

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We examined the prevalence of HIV-associated cutaneous disorders as well as the frequency and efficiency of UV-radiation in HIV-infected patients by evaluating the clinical records of 1310 patients seen between and 1994 and 1996. 41 patients were treated with UVB-radiation and 4 patients with UVA1-radiation, while three patients received PUVA-therapy. UV-radiation proved to be efficient and safe in the treatment of pruritic papular eruption, atopic dermatitis and psoriasis. Although some in vitro studies and studies with transgenic mice have suggested a negative impact of UV radiation on the immunosystem of HIV-positive patients, no progression of the HIV infection due to phototherapy has been proven.

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“…[1][2][3][4][5][6] Ultraviolet-B light from artificial and natural sources was first shown to enhance HIV growth in experiments using cell culture systems. 7,8 In vivo studies using transgenic mice that express the HIV longterminal-repeat promoter linked to reporter genes further indicated that sunlight and artificial UV-B in doses as low as 9 mJ/ cm 2 can potently stimulate viral replication in the skin.…”

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confidence: 99%