Identification of a Human Immunodeficiency Virus Type 1 TAR Binding Protein in Human Hepatoblastoma HepG2 Cells That<i>Trans</i>-Activates HIV-1 LTR-Directed Gene Expression

Pizzella, T; Banerjee, Ranjit

doi:10.1089/dna.1994.13.67

Cited by 9 publications

(3 citation statements)

References 51 publications

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“…Using linker-scanning mutational analysis, we have identified several domains of the HIV-1 LTR responsible for basal as well as TCDD-stimulated CAT expression. We find that expression directed by the HIV-1 LTR is high in mouse hepatoma cells, in agreement with previous observations in human hepatoma cell lines (49)(50)(51), this suggests that the liver may be a primary virus reservoir. Mutation of the NFICB binding sites eliminates CAT expression, confirming the absolute requirement for NFiB.…”

Section: Discussionsupporting

confidence: 92%

Dioxin activates HIV-1 gene expression by an oxidative stress pathway requiring a functional cytochrome P450 CYP1A1 enzyme.

Yao

Hoffer

Chang

et al. 1995

Environ Health Perspect

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We have studied the effect of several environmental chemicals on the transient expression of a chloramphenicol acetyltransferase (cat) reporter gene linked to the promoter sequences in the long terminal repeat (LTR) of the human immunodeficiency virus type 1 (HIV-1). Aflatoxin B1, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) and benzo[a]pyrene cause a significant increases in CAT expression in mouse hepatoma Hepa-1 cells. The induction of CAT after TCDD treatment is abolished by administration of N-acetyl-L-cysteine or 2-mercaptoethanol and does not take place in a mutant cell line that lacks CYP1A1 enzymatic activity. Linker-scanning mutational analysis of transcription factor binding sites in the promoter revealed that both the NF kappa B and an adjacent aromatic hydrocarbon response element (AhRE) are required for TCDD-dependent CAT expression. In addition, mutation of the NFAT/AP-1 binding sites in the negative regulatory region of the promoter increases the magnitude of the TCDD effect. We conclude that induction of a functional CYP1A1 monooxygenase by TCDD stimulates a pathway that generates thiol-sensitive reactive oxygen intermediates which, in turn, are responsible for the TCDD-dependent activation of genes linked to the LTR. These data might provide an explanation for findings that TCDD increases infectious HIV-1 titers in experimental systems and for epidemiologic reports suggesting that exposure to aromatic hydrocarbons, such as found in cigarette smoke, is associated with an acceleration in AIDS progression.Imagesp366-aFigure 2.Figure 3.Figure 4.Figure 5.

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Section: Discussionsupporting

confidence: 92%

Dioxin activates HIV-1 gene expression by an oxidative stress pathway requiring a functional cytochrome P450 CYP1A1 enzyme.

Yao

Hoffer

Chang

et al. 1995

Environ Health Perspect

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“…Nuclear and cytoplasmic extracts from each set of HepG2 treatment groups were prepared from 1 ϫ 10 7 cells, for analysis by electrophoretic mobility shift assay using a previously published protocol with some modifications. 27,28 Briefly, cells were washed in ice cold phosphate-buffered saline (PBS) and swelled in 4 vol of Extraction Buffer A (10 mmol/L HEPES, pH 7.9; 10 mmol/L NaCl; 3 mmol/L MgCl 2 ; 0.2 mmol/L ethylenediaminetetraacetic acid [EDTA]; 1 mmol/L dithiothreitol [DTT]; 0.4 mmol/L phenylmethyl sulfonyl fluoride [PMSF]; 1 g/mL antipain; and 1 g/mL leupeptin) for 30 minutes at 4°C and collected by centrifugation at 2,000 rpm for 5 minutes. The cell pellets were resuspended in 2 vol of Buffer B (20 mmol/L HEPES, pH 7.9; 10 mmol/L NaCl; 3 mmol/L MgCl 2 ; 0.1% Nonidet P-40; 10% glycerol; 0.2 mmol/L EDTA; 1 mmol/L DTT; 0.4 mmol/L PMSF; 1 g/mL antipain; and 1 g/mL leupeptin) and dounced 6 to 8 times in a 2-mL homogenizer.…”

Section: Methodsmentioning

confidence: 99%

Effects of carcinogen-induced transcription factors on the activation of hepatitis B virus expression in human hepatoblastoma HepG2 cells and its implication on hepatocellular carcinomas

Banerjee¹,

Caruccio²,

Zhang³

et al. 2000

Hepatology

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“…Moreover, HIV infection of multiple liver cell populations including hepatocytes and hepatic stellate cells has been reported [25]–[28], [30]. Previous studies have reported basal LTR activation in HepG2 hepatoma cells [68], [69], although other cell types more relevant to HCV replication and HIV/HCV co-infection have not been rigorously evaluated.…”

Section: Discussionmentioning

confidence: 99%

Effects of HCV on Basal and Tat-Induced HIV LTR Activation

et al. 2013

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Hepatitis C virus (HCV) co-infection occurs in ∼30–40% of the HIV-infected population in the US. While a significant body of research suggests an adverse effect of HIV on HCV replication and disease progression, the impact of HCV on HIV infection has not been well studied. Increasing data suggest that hepatocytes and other liver cell populations can serve as reservoirs for HIV replication. Therefore, to gain insight into the impact of HCV on HIV, the effects of the HCV Core protein and infectious hepatitis C virions were evaluated on basal and Tat-induced activation of the HIV long terminal repeat (LTR) in hepatocytes. The HIV LTR was highly induced by the HIV transactivator protein Tat in hepatocytes. Activation varied according to the number of NF-kB binding sites present in the LTRs from different HIV subtypes. Involvement of the NF-kB binding pathway in LTR activation was demonstrated using an NF-kB inhibitor and deletion of the NF-kB binding sites. TNFα, a pro-inflammatory cytokine that plays an important role in HIV pathogenesis, also induced LTR activity in hepatocytes. However, HIV LTR activity was suppressed in hepatocytes in the presence of HCV Core protein, and the suppressive effect persisted in the presence of TNFα. In contrast, infectious hepatitis C virions upregulated HIV LTR activation and gene transcription. Core-mediated suppression remained unaltered in the presence of HCV NS3/4A protein, suggesting the involvement of other viral/cellular factors. These findings have significant clinical implications as they imply that HCV could accelerate HIV disease progression in HIV/HCV co-infected patients. Such analyses are important to elucidate the mechanisms by which these viruses interact and could facilitate the development of more effective therapies to treat HIV/HCV co-infection.

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Identification of a Human Immunodeficiency Virus Type 1 TAR Binding Protein in Human Hepatoblastoma HepG2 Cells ThatTrans-Activates HIV-1 LTR-Directed Gene Expression

Cited by 9 publications

References 51 publications

Dioxin activates HIV-1 gene expression by an oxidative stress pathway requiring a functional cytochrome P450 CYP1A1 enzyme.

Dioxin activates HIV-1 gene expression by an oxidative stress pathway requiring a functional cytochrome P450 CYP1A1 enzyme.

Effects of carcinogen-induced transcription factors on the activation of hepatitis B virus expression in human hepatoblastoma HepG2 cells and its implication on hepatocellular carcinomas

Effects of HCV on Basal and Tat-Induced HIV LTR Activation

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