HIV-1 promoter activation following an oxidative stress mediated by singlet oxygen

Legrand-Poels, Sylvie; Hoebeke, Maryse; Vaira, Dolores; Rentier, Bernard; Piette, Jacques

doi:10.1016/1011-1344(93)80020-a

Cited by 38 publications

(8 citation statements)

References 56 publications

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“…6). The intensities of the reactivations observed are similar to those described previously for rose-Bengal-mediated phototreatment [38]. For an equivalent cytotoxic effect, the reverse transcriptase stimulation factor for U1 cells appears to be double that for ACH-2 cells.…”

Section: Photosensitization Mediated By Methylene Blue Reactivates Hisupporting

confidence: 86%

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NF-kappa B Transcription Factor and Human Immunodeficiency Virus Type 1 (HIV-1) Activation by Methylene Blue Photosensitization

Piret¹,

Legrand-Poels²,

Sappey³

et al. 1995

Eur J Biochem

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Reactive oxygen species like hydrogen peroxide (H202) have been shown to serve as messengers in the induction of NF-KB and then in the activation and replication of HIV-1 in human cells. Because singlet oxygen ('0,) is another very important reactive oxygen species whose action in transcription factor activation is totally undetermined, we started to investigate its role in both NF-KB and HIV-1 activation. For provoking unbalanced redox conditions, '0, was generated by photosensitization using methylene blue as photosensitizer. Lymphocytes or monocytes (ACH-2 or U1 respectively) latently infected with HIV-1 were treated by photosensitization mediated by methylene blue and the production of reactive oxygen species was monitored through their cytotoxic effect in infected cells. The generation of '0, by methylene blue turns out to be very efficient in inducing NF-KB as a heterodimer composed of the p50 and p65 subunits. This induction appears specific since other transcription factors like AP-1 are only weakly activated by this treatment. In comparison with other inducing treatments such as phorbol esters or tumor necrosis factor alpha (TNF-a), the methylene-blue-mediated activation of NF-KB is slow, becoming optimal 180 min after treatment. These kinetic data were obtained by following, on the same samples, both the emergence of NF-KB in the nucleus and the disappearance of IKB-a in the cytoplasmic extracts. Conjugated with the induction of this transcription factor, HIV-1 reactivation from these latently infected cells was also observed by the measurement of reverse transcriptase activity in the cell supernatants. These data allow us to postulate that '0, is a biologically important reactive oxygen species which could play a role in the establishment of oxidative stress conditions leading to HIV-1 activation via the presence of NF-KB in the nucleus of infected cells.

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Section: Photosensitization Mediated By Methylene Blue Reactivates Hisupporting

confidence: 86%

“…For experiments with cycloheximide, this drug was added immediately after illumination and was present in the culture medium until protein extraction. Rose-Bengal-mediated photosensitization of ACH-2 and U1 cells is described elsewhere [38].…”

Section: Methodsmentioning

confidence: 99%

NF-kappa B Transcription Factor and Human Immunodeficiency Virus Type 1 (HIV-1) Activation by Methylene Blue Photosensitization

Piret¹,

Legrand-Poels²,

Sappey³

et al. 1995

Eur J Biochem

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“…An exhaustive list of host factors interacting with HIV-1 LTR is summarized by Pereira et.al [16]. These regulatory factors may vary in response to stimuli like hyperthermia, oxidative stress and infections such as that of mycobacteria [23], [31], [32], [33]. There are emerging evidences that HIV-TB coalition may also be explained by M.tb factors promoting HIV-1 LTR activity.…”

Section: Introductionmentioning

confidence: 99%

Mycobacterial and HIV Infections Up-Regulated Human Zinc Finger Protein 134, a Novel Positive Regulator of HIV-1 LTR Activity and Viral Propagation

et al. 2014

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BackgroundConcurrent occurrence of HIV and Tuberculosis (TB) infections influence the cellular environment of the host for synergistic existence. An elementary approach to understand such coalition at the molecular level is to understand the interactions of the host and the viral factors that subsequently effect viral replication. Long terminal repeats (LTR) of HIV genome serve as a template for binding trans-acting viral and cellular factors that regulate its transcriptional activity, thereby, deciding the fate of HIV pathogenesis, making it an ideal system to explore the interplay between HIV and the host.Methodology/Principal FindingsIn this study, using biotinylated full length HIV-1 LTR sequence as bait followed by MALDI analyses, we identified and further characterized human-Zinc-finger-protein-134 (hZNF-134) as a novel positive regulator of HIV-1 that promoted LTR-driven transcription and viral production. Over-expression of hZNF-134 promoted LTR driven luciferase activity and viral transcripts, resulting in increased virus production while siRNA mediated knockdown reduced both the viral transcripts and the viral titers, establishing hZNF-134 as a positive effector of HIV-1. HIV, Mycobacteria and HIV-TB co-infections increased hZNF-134 expressions in PBMCs, the impact being highest by mycobacteria. Corroborating these observations, primary TB patients (n = 22) recorded extraordinarily high transcript levels of hZNF-134 as compared to healthy controls (n = 16).Conclusions/SignificanceWith these observations, it was concluded that hZNF-134, which promoted HIV-1 LTR activity acted as a positive regulator of HIV propagation in human host. High titers of hZNF-134 transcripts in TB patients suggest that up-regulation of such positive effectors of HIV-1 upon mycobacterial infection can be yet another mechanism by which mycobacteria assists HIV-1 propagation during HIV-TB co-infections. hZNF-134, an uncharacterized host protein, thus assumes a novel regulatory role during HIV-host interactions. Our study provides new insights into the emerging role of zinc finger proteins in HIV-1 pathogenesis.

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“…Various genes have been described to be activated upon exposure of cells to singlet oxygen. For example, singlet oxygen can activate the HIV long terminal repeat integrated into cellular DNA of epithelial cells [13]. Interestingly, UV light has also been described to activate HIV gene expression [14].…”

Section: Introductionmentioning

confidence: 99%

Singlet oxygen induces collagenase expression in human skin fibroblasts

Scharffetter‐Kochanek

et al. 1993

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Singlet oxygen generated in a dark reaction by thermodissociation of an endoperoxide (NDPOJ elicits an increase in mRNA of interstitial collagenase (MMP-1) in cultured human fibroblasts. The effect is enhanced in deuterium oxide-based medium and is abolished in the presence of non-toxic doses of sodium azide. In contrast, the mRNA level of the tissue inhibitor of metalloproteinases (TIMP-1) remains unaltered under these experimental conditions. These observations support the suggestion that an unbalanced synthesis of collagenase and TIMP reported to occur following UV-A irradiation or during inflammatory conditions may be mediated by singlet oxygen.

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HIV-1 promoter activation following an oxidative stress mediated by singlet oxygen

Abstract: Various biological processes, such as photosensitization or inflammatory reactions, can generate singlet oxygen ( 1 O 2 ) as one of the major oxidative species.

Cited by 38 publications

References 56 publications

NF-kappa B Transcription Factor and Human Immunodeficiency Virus Type 1 (HIV-1) Activation by Methylene Blue Photosensitization

NF-kappa B Transcription Factor and Human Immunodeficiency Virus Type 1 (HIV-1) Activation by Methylene Blue Photosensitization

Mycobacterial and HIV Infections Up-Regulated Human Zinc Finger Protein 134, a Novel Positive Regulator of HIV-1 LTR Activity and Viral Propagation

Singlet oxygen induces collagenase expression in human skin fibroblasts

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