Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0021051 (immunodeficiency)
71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We developed a sensitive vector system for the analysis of weak promoter activities. This promoter assay is based on the transcriptional activator protein, Tat, of human immunodeficiency virus type 1 (HIV-1). High-level expression of HIV requires activation in trans by Tat of the promoter in the long terminal repeat (LTR). Here we describe the construction of a promoterless pTat vector. Foreign promoter elements can be inserted upstream from the tat gene, and expression of Tat protein is measured in trans on a co-transfected LTR-CAT reporter plasmid. We show that this binary system is more sensitive than standard pCAT reporter assays.
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PMID:A sensitive promoter assay based on the transcriptional activator Tat of the HIV-1 virus. 803 9

The long terminal repeat (LTR) of human immunodeficiency virus type 1 (HIV-1) is activated under different conditions including heat shock. By using transient transfection assay, we have compared the thermal activation of HIV-1 LTR to that of the promoter of the gene encoding the human stress protein hsp70 which is under the control of the heat shock transcription factor HSF. In these assays, the chloramphenicol acetyl transferase (Cat) gene was used as a reporter gene. Several parameters of the heat stress were analyzed such as the temperature, the duration of heat stress and that of the recovery period. Under every condition tested, we have found that the kinetics of activation of both promoters were very similar. In addition, both showed a similar inhibition by actinomycin D. These results were compared to those obtained with a DNA construct containing the early promoter of SV-40 virus coupled to the Cat gene. In this case, no heat-mediated accumulation of CAT protein was observed, indicating that the transcriptional activation of HIV-1 LTR by heat shock is specific. HIV-1 LTR contains two NF-kappa B binding elements, involved in the activation of this promoter during oxidative stress, which are sequence related to the heat shock element HSE. However, under all the heat shock conditions tested, we have been unable to detect the binding of any protein to kappa B elements, suggesting that this site is not directly involved in the thermal activation of HIV-1 LTR. These results indicate that the thermal transcriptional activation of HIV-1 LTR and hsp70 promoters occurs through different mechanisms that are triggered by similar heat shock conditions.
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PMID:The kinetics of HIV-1 long terminal repeat transcriptional activation resemble those of hsp70 promoter in heat-shock treated HeLa cells. 781 29

The activation of human immunodeficiency virus type 1 (HIV-1) expression in latently infected cells by exogenous agents is believed to be important in the progression of AIDS. Most factors that are known to activate HIV-1 gene expression increase the binding of NF-kappa B or NF-kappa B-like transcription factors to the HIV-1 core enhancer region. In this report, we demonstrate that retinoic acid (RA) treatment of promonocytic U937 cells stimulates expression from the simian immunodeficiency virus (SIVmac) long terminal repeat (LTR). Furthermore, RA and phorbol 12-myristate 13-acetate (PMA) synergistically stimulated both SIVmac and HIV-1 LTRs to levels of expression comparable to that achieved by the viral transactivator Tat. The cis-acting elements required for a response to RA and PMA cotreatment are located between nucleotides -50 and +1 of SIVmac and between nucleotides -83 and +80 of HIV-1. Thus, the synergistic stimulation induced by RA and PMA is NF-kappa B independent. Analysis of deletion mutants of the SIVmac LTR demonstrates that RA and PMA stimulation cooperates with NF-kappa B and Sp1. An SIVmac LTR-reporter gene construct [pLTR(-50/+466)CAT] lacking NF-kappa B and Sp1 binding sites was not activated by Tat in untreated cells but was activated in cells that were cotreated with RA and PMA. Furthermore, gel retardation assays demonstrated that RA treatment causes a change in the pattern of a cellular factor(s) which binds to the -50 through +1 region of the SIVmac LTR. These data suggest that RA induces a PMA-activatable cellular factor that cooperates with NF-kappa B, Sp1, or Tat to stimulate LTR-directed transcription.
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PMID:Synergistic activation of simian immunodeficiency virus and human immunodeficiency virus type 1 transcription by retinoic acid and phorbol ester through an NF-kappa B-independent mechanism. 808 95

We have previously described the apparent acquisition by human herpesvirus 6 (HHV-6) of the multifunctional rep gene of the helper-dependent human parvovirus adeno-associated virus type 2 (AAV-2). We report here that HHV-6 is a full helper virus for AAV-2 replication, suggesting a mechanism for transfer of the rep gene between the two viruses by recombination of replicative intermediates. The HHV-6 rep gene cloned under control of the human cytomegalovirus immediate early promoter complemented replication of a rep-deficient AAV-2 genome. In cotransfection experiments with heterologous promoters linked to the CAT reporter gene, HHV-6 rep activated the human immunodeficiency virus (HIV) long terminal repeat (LTR) in fibroblast cell lines but not in T-cells. In contrast, AAV-2 rep inhibited HIV LTR activity in both fibroblast and T-cell lines. The effect of HHV-6 and AAV-2 rep genes on the HIV LTR was independent of the NF-kappa B, Sp1, and TATA box elements. These results suggest that HHV-6 Rep is a multifunctional regulatory protein with properties related to, but distinct from, those of AAV-2 Rep.
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PMID:Human herpesvirus 6 (HHV-6) is a helper virus for adeno-associated virus type 2 (AAV-2) and the AAV-2 rep gene homologue in HHV-6 can mediate AAV-2 DNA replication and regulate gene expression. 809 61

Previously it has been demonstrated that the human immunodeficiency virus type 1 (HIV-1) Tat protein mediates induction of the HIV-1 env expression through a TAR-independent manner in heterologous and homologous promoter systems (Kim and Risser, 1993, J. Virol. 67, 239; Kim and Panganiban, 1993, J. Virol. 67, 3739). To further explore the transactivation of HIV-1 env gene, I examined expression of the env, the bacterial CAT, and the firefly luciferase genes from a heterologous promoter, the major immediate-early promoter (MIEP) of murine cytomegalovirus (MCMV). Here we show that Tat augments gene expression from the MCMV MIEP only when linked to the env gene. Surprisingly, in contrast to the expression from an HIV-1 LTR lacking the TAR element, TAR-independent transactivation of env gene expression from MCMV MIEP did not require the full length Tat protein. In addition, deletion of the previously identified cis-acting Tat-responsive element in env did not affect Tat transactivation of the env gene expression. Thus, there are multiple distinct elements that mediate Tat responsiveness in the absence TAR.
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PMID:Requirement of the human immunodeficiency virus type 1 env gene sequence for TAR-independent trans activation by Tat from the major immediate-early promoter of murine cytomegalovirus. 809 34

HHV-6 infection has been associated with several malignancies including non-Hodgkin's lymphoma and Hodgkin's disease by the presence of high antibody titer and/or the presence of HHV-6 DNA. To understand their oncogenic potential, SalI restriction fragments from HHV-6 strain U1102 were transfected into NIH3T3 cells to assess transforming ability. A 3.9-kbp SalI-L DNA fragment spanning the junction of the direct repeat left (DRL) and unique long segment (UL) regions of HHV-6 induced foci of morphologically altered cells. The SalI-L transformed NIH3T3 focal lines induced tumors in nude mice within 2 weeks. The retention of HHV-6 specific DNA observed in SalI-L transformed cells and their tumor-derived lines suggest a possible maintenance function. Since both HHV-6 infection as well as transforming fragments from other DNA viruses have been shown to transactivate the human immunodeficiency virus type 1 (HIV-1) long terminal repeat (LTR), SalI-L was examined for transactivation activity. SalI-L up-regulated HIV-1 LTR CAT 10-15 fold in both monkey CV-1 and human T Jurkat cells. The further study of the SalI-L transforming fragment exhibiting transactivation of HIV-1 LTR will elucidate whether these two activities are encoded by a single gene and will aid in the understanding of the interaction between HHV-6 and HIV-1 as it relates to progression of AIDS and/or AIDS-related malignancies.
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PMID:A transforming fragment within the direct repeat region of human herpesvirus type 6 that transactivates HIV-1. 813 19

CD8+ T cells from naturally infected disease-resistant sooty mangabeys (Cercocebus atys) secrete a soluble factor which inhibits the in vitro replication of the simian immunodeficiency virus (SIV). To gain further insight on the mechanism(s) involved, CD8+ effector T cells and target cells from sooty mangabeys were immortalized and cloned. The target cells were then stably transfected with an SIV-LTR-CAT construct or with the parental CAT plasmid as a control. A quantitative RT-PCR method, providing the necessary sensitivity, was developed to monitor the influence of the cloned CD8+ T cells on the CATmRNA contained in the target cells. It could be demonstrated that a soluble factor was secreted by the cloned CD8+ T cells from sooty mangabeys, which appeared to regulate CATmRNA activity in a dose-dependent and reversible manner. Kinetic experiments showed that the CATmRNA transcriptional activity was initially augmented at 30 min postcoculture and was followed by a marked decrease in transcriptional activity after a few hours. This immediate early response could be mitigated utilizing H7, Calmodulin, or PDTC (a pyrrolidone derivative of dithiocarbamate), suggesting that the pathway was protein kinase-dependent and that the NF-kappa B site may be involved. The inhibitory effect could also be overcome using a protein synthesis inhibitor, suggesting that protein synthesis was needed to negatively regulate CATmRNA activity and hence SIV promoter activity.
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PMID:Biphasic in vitro regulation of retroviral replication by CD8+ cells from nonhuman primates. 815 36

From the sera of patients with advanced cancer, a novel factor called SDF (serum-derived factor) was partially purified. SDF was shown to stimulate transcription from the long terminal repeat (LTR) of human immunodeficiency virus type 1 (HIV-1) by transient CAT assay. It did not stimulate gene expression of various control promoters including Rous sarcoma virus, human c-fos, c-myc, c-H-ras and chicken beta-actin genes. The SDF preparation did not contain any detectable TNF-alpha or TNF-beta, and differed in its physicochemical properties from TNFs. We concluded that SDF might be a novel factor associated with the clinical features of advanced cancer. It is speculated that SDF might have some role in disease progression of AIDS as well as in the development of the cachectic conditions in AIDS associated with malignancies.
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PMID:Identification in the sera from patients with advanced cancer of a factor which stimulates gene expression from human immunodeficiency virus type 1. 823 10

The transcriptional activity of human immunodeficiency virus type 1 (HIV-1) is affected by many cellular factors. Homologies near the HIV-1 initiator region to the DNA-binding sequences of YY1, a multifunctional transcription factor known to regulate diverse viral and cellular promoters, suggested that YY1 might regulate HIV-1. Antibody to YY1 blocked the formation of complexes by HeLa cell nuclear extract and a DNA oligonucleotide encoding the HIV-1 initiator region. HIV-1 long terminal repeat (LTR) expression, as measured the expression of a transfected LTR-CAT reporter gene, was repressed more than 12-fold by the cotransfection of a YY1 expression vector. HIV-1 production by both COS-1 and CEM cells after transfection of an infectious molecular HIV-1 clone was repressed 7- to 20-fold by cotransfection of a YY1 expression vector. HIV-1 production was also decreased threefold in a CD4-positive lymphocyte cell line chronically infected with HIV-1 (8E5) after transfection of YY1. In situ hybridization studies confirmed that YY1 reduced HIV-1 RNA expression. YY1 may play an important role in the regulation of HIV-1 LTR expression in vivo and virus production by infected cells.
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PMID:Human transcription factor YY1 represses human immunodeficiency virus type 1 transcription and virion production. 828 93

The expression of human immunodeficiency virus type 1 (HIV-1) is enhanced after cell activation because of the interaction of cell-encoded nuclear factors that interact with binding sites in the long terminal repeats (LTRs). Here we studied the contribution of cell type-specific activation signals to differences in cytotropism of HIV-1 variants. Four closely related molecular HIV-1 clones with distinct biological phenotypes and different capacities to replicate in primary monocyte-derived macrophages (MDMs) or T cell lines were used. Sequence analysis of these LTRs revealed variation in functionally important regions. Adaptation of virus variants to particular host cells by differences in LTR responsiveness was analyzed. LTR-CAT constructs were transiently transfected in T cells that were stimulated with T cell-specific activation signals such as combinations of anti-CD3 or anti-CD28 MoAB or in primary monocytes that were stimulated with IL-3, IL-4, or GM-CSF. No differences in responsiveness to cell type-specific signals were demonstrated. To further elucidate the level of restriction in cell tropism, transfection of four full-length infectious molecular HIV-1 clones into 5-day cultured MDMs was performed. From all clones, competent virus could be rescued from MDMs by coculture with PHA-stimulated PBLs. However, following cell-free inoculation, proviral DNA could be detected by PCR analysis only in monocytes exposed to HIV-1 clones that previously were shown to establish productive infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early replication steps but not cell type-specific signalling of the viral long terminal repeat determine HIV-1 monocytotropism. 836 71


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