Activation of the Human Immunodeficiency Virus Promoter by Uva Radiation in Combination With Psoralens or Angelicins

Zmudzka, Barbara Z.; Strickland, Amparo G.; Miller, Sharon A.; Valerie, Kristoffer; Dall’Acqua, Francesco; Beer, Janusz Z.

doi:10.1111/j.1751-1097.1993.tb09553.x

Cited by 32 publications

(13 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our studies support the concept that UV exposure can activate HIV gene expression as shown previously in transfected or latently infected cells (1)(2)(3)(4)(5)(6), and demonstrate for the first time that UVB-inducible HIV activation occurs in skin of seropositive individuals. The mechanism by which UV activates HIV gene expression has not been elucidated precisely, although pathways involving NFB (20)(21)(22) and p38 MAP kinase (23-25) have been implicated.…”

Section: Discussionsupporting

confidence: 90%

“…Concern about a detrimental relationship between ultraviolet radiation and HIV infection was triggered by cell culture (1)(2)(3)(4)(5)(6) and transgenic animal studies (7)(8)(9) that have shown ul- ¶Posted on the website on 17 traviolet B (UVB), ultraviolet C and psoralens plus ultraviolet A (PUVA) treatments to upregulate HIV gene expression, activate latent HIV or promote HIV replication (or all of them). Alerted by these findings, clinical investigators studied serial cases of HIV-infected patients treated for psoriasis, eosinophilic folliculitis or pruritus, with either UVB phototherapy or PUVA photochemotherapy (10)(11)(12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Activation of HIV in Human Skin by Ultraviolet B Radiation and its Inhibition by NFκB Blocking Agents¶

Breuer-McHam¹,

Simpson²,

Dougherty³

et al. 2001

Photochem Photobiol

View full text Add to dashboard Cite

To determine whether ultraviolet B (UVB) irradiation leads to activation of HIV in human skin, we conducted prospective and controlled studies in two academic medical centers in Texas from July 1995 to April 1999. HIV-positive patients with UV-treatable skin diseases were enrolled at each center, 18 subjects at one and 16 at the other. In one center, specimens from lesional and nonlesional skin biopsies were taken before and after sham- or UVB-irradiation administered in vivo or in vitro. In the other center, UVB phototherapy was administered three times weekly and specimens from skin biopsies were taken before and after 2 weeks (six treatments). Cutaneous HIV load was assessed using reverse transcriptase-polymerase chain reaction and reverse transcriptase-polymerase chain reaction in situ hybridization. UVB irradiation led to a 6-10-fold increase in the number of HIV in skin. To ascertain a role for nuclear factor kappa B (NFkappaB) in UVB-inducible HIV activation, two types of blockers, NFkappaB oligonucleotide decoy and sodium salicylate, were tested; each inhibited UVB-inducible HIV activation in skin partially. We conclude that UVB irradiation leads to increased numbers of HIV in human skin via processes that include release of cytoplasmic NFkappaB.

show abstract

Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Activation of HIV in Human Skin by Ultraviolet B Radiation and its Inhibition by NFκB Blocking Agents¶

Breuer-McHam¹,

Simpson²,

Dougherty³

et al. 2001

Photochem Photobiol

View full text Add to dashboard Cite

show abstract

“…Previous studies have shown that PUVA can activate the HIV promoter in HIVcarMeLa cells (12). The UVA light dose response and kinetics of the HIV promoter activation are shown in Fig.…”

Section: Resultsmentioning

confidence: 88%

Photosensitized Decontamination of Blood with the Silicon Phthalocyanine Pc 4: No Activation of the Human Immunodeficiency Virus Promoter

Zmudzka

Strickland

Beer

et al. 1997

Photochem & Photobiology

Self Cite

View full text Add to dashboard Cite

Photochemical decontamination of red blood cell concentrates (RBCC) with the silicon phthalocyanine Pc 4 and red light is being studied to enhance the viral safety of blood transfusion. Recent reports indicate that treatments with radiation and various phototsensitizing agents can activate the promoter of human immunodeficiency virus (HIV). This raises the possibility that an inadequate, sublethal photochemical treatment of RBCC could induce HIV in latently infected cells. This question has been addressed using HeLa cells stably transfected with the chloramphenicol acetyl transferase gene under the control of the HIV promoter. In control studies, 8-methoxypsoralen (8-MOP) excited by UVA light caused activation of the HIV promoter in a dose- and time-dependent manner. At 0.1 microgram/mL of 8-MOP, maximal activation occurred with 18 J/cm2, 30 h after light exposure, With Pc 4 at 20 nM, over 90% of HeLa cells were killed after 24 h when exposed to 1 J/cm2 of red light. During that time interval and over a wide range of light doses no activation of the HIV promoter occurred. It is concluded that RBCC sterilization with Pc 4 and red light is unlikely to induce HIV production in latently infected cells.

show abstract

“…The specific therapeutic efficacies of MAs and ICLs are not well characterized. Zmudzka et al (20) have studied how the incident dose required for angelicins to induce 10% HIV promoter activity induction correlates to the DNA binding constant (20). Angelicins are limited by their structures to the formation of monoadducts.…”

Section: Discussionmentioning

confidence: 99%

UVA and UVB‐Induced 8‐Methoxypsoralen Photoadducts and a Novel Method for their Detection by Surface‐Enhanced Laser Desorption Ionization Time‐of‐Flight Mass Spectrometry (SELDI‐TOF MS)

Buhimschi

Gasparro

2013

Photochem & Photobiology

View full text Add to dashboard Cite

UVA-activated psoralens are used to treat hyperproliferative skin conditions due to their ability to form DNA photoadducts, which impair cellular processes and may lead to cell death. Although UVA (320-400 nm) is more commonly used clinically, studies have shown that UVB (280-320 nm) activation of psoralen can also be effective. However, there has been no characterization of UVB-induced adduct formation in DNA alone. As psoralen derivatives have a greater extinction coefficient in the UVB region (11 800 cm(-1) M(-1) at 300 nm) compared with the UVA region (2016 cm(-1) M(-1) at 365 nm), a greater extent of adduct formation is expected. SELDI-TOF, a proteomic technique that combines chromatography with mass spectrometry, was used to detect photoadduct formation in an alternating A-T oligonucleotide. 8-Methoxypsoralen (8-MOP) and DNA solutions were irradiated with either UVA or UVB. An adduct peak was obtained with SELDI-TOF. For UVB-activated 8-MOP, the extent of adducts was three times greater than for UVA. HPLC ESI-MS analysis showed that UVB irradiation yielded high levels of 3,4-monoadducts (78% of total adducts). UVA was more effective than UVB at conversion of 4',5'-monoadducts to crosslinks (17% vs 4%, respectively). This report presents a method for comparing DNA binding efficiencies of interstrand crosslink inducing agents.

show abstract

Activation of the Human Immunodeficiency Virus Promoter by Uva Radiation in Combination With Psoralens or Angelicins

Cited by 32 publications

References 25 publications

Activation of HIV in Human Skin by Ultraviolet B Radiation and its Inhibition by NFκB Blocking Agents¶

Activation of HIV in Human Skin by Ultraviolet B Radiation and its Inhibition by NFκB Blocking Agents¶

Photosensitized Decontamination of Blood with the Silicon Phthalocyanine Pc 4: No Activation of the Human Immunodeficiency Virus Promoter

UVA and UVB‐Induced 8‐Methoxypsoralen Photoadducts and a Novel Method for their Detection by Surface‐Enhanced Laser Desorption Ionization Time‐of‐Flight Mass Spectrometry (SELDI‐TOF MS)

Contact Info

Product

Resources

About