Disease relevance of Genes, Viral

• HIV-1 encodes a potent trans-activator protein, tat, which is essential for viral gene expression [1].
• The first mechanism operates in undifferentiated cells to block expression of M-MuLV and other exogeneously acquired viral genes, such as SV40 and polyoma virus, and does not depend on DNA methylation [2].
• Herpesviruses establish latent infections in neurons during which only one viral gene (LAT) is expressed, thus the LAT promoter may express foreign genes in latently infected CNS cells [3].
• These levels are similar to those obtained by the tat gene product, the HIV trans-activating factor responsible for enhancing viral gene expression [4].
• A viral gene product has not been definitively linked to these malignant diseases, although an EBV nuclear antigen(s) (EBNA) seems to be ubiquitous in EBV-infected cells; indeed, the detection of EBNA by immunofluorescence is often taken as an indication of the presence of the viral genome [5].

High impact information on Genes, Viral

• This study demonstrates that one of the viral genes necessary for this inhibition, the crmA gene (a cytokine response modifier gene), encodes a serpin that is a specific inhibitor of the interleukin-1 beta converting enzyme [6].
• This normal cellular protein (NCP98) was shown to be structurally related to P140, sharing the majority of 35S-methionine-labeled tryptic peptides with the viral gene product P140 [7].
• We conclude that posttranscriptional regulation of cII by host and viral genes is critical for the choice of a developmental pathway [8].
• The SV40 large T antigen is a multifunctional protein presumed to represent a single translation product of the early viral genes [9].
• Several lines of evidence, including complementation of glycoprotein processing defects by fusion with uninfected wild-type cells, indicate that the immunoselected variants have stably inherited membrane synthesis abnormalities that are encoded by cellular rather than by viral genes [10].

Chemical compound and disease context of Genes, Viral

• Similarly, the viral gene product pp60src, which is responsible for cellular transformation by avian sarcoma virus (ASV), phosphorylates itself and immunoglobulin directed against pp60src at tyrosine residues [11].
• We now report that the formation of the 40S--Met-tRNAfMet initiation complex is inhibited in cytoplasmic extracts derived from vaccinia virus-infected cells exposed to cordycepin to block viral gene expression [12].
• This was achieved by using vaccinia recombinants encoding viral genes expressed at different stages of the virus replicative cycle, a structural glycoprotein gB (vac.gB) and the major 72-kD immediate early nonstructural protein (vac.IE) of HCMV, combined with limiting dilution analysis of the CTL response [13].
• The plasmids consisted of fusions between the E. coli DNA encoding the first 13 amino acids of the trp operon leader protein and viral genes encoding the 3Cpro and 3Dpol polypeptides [14].
• Mutations in the viral gene coding for the thymidine kinase (ATP:thymidine 5'-phosphotransferase, EC 2.7.1.75) induced by herpes simplex virus have been obtained by selection of virus resistant to bromodeoxyuridine when grown in thymidine-kinase-deficient LMTK- mouse cells [15].

Biological context of Genes, Viral

• Increased Notch1 signaling, but not Notch2, causes a dramatic down-modulation of HPV-driven transcription of the E6/E7 viral genes, through suppression of AP-1 activity by up-regulation of the Fra-1 family member and decreased c-Fos expression [16].
• The Tat protein of human immunodeficiency virus type 1 (HIV-1) trans-activates viral gene expression and is obligatory for virus replication [17].
• A key activator of lytic infection is a virion protein called VP16, which, upon infection of a permissive cell, forms a transcriptional regulatory complex with two cellular proteins - the POU-domain transcription factor Oct-1 and the cell-proliferation factor HCF-1 - to activate transcription of the first set of expressed viral genes [18].
• Although being able to stimulate both types of genes, we find that the E1A regulatory protein enhances viral gene expression approximately 10 times more than beta-globin gene expression [19].
• Thus, the progression of resting B lymphocytes into the G1 phase of the cell cycle can be reconstituted in the absence of virus by the cooperation of two of the six viral genes required for immortalization [20].

Anatomical context of Genes, Viral

• Two HIV proteins, Nef and Tat, increase T cell activity, but a requirement of integration for viral gene expression would preclude a role for these proteins in resting cells [21].
• We show that the full length HPV E2 protein acts as a potent transcriptional activator of viral gene expression in both normal and immortalized keratinocytes [22].
• U94 of human herpesvirus 6 is expressed in latently infected peripheral blood mononuclear cells and blocks viral gene expression in transformed lymphocytes in culture [23].
• The accessory protein, Vpr, is a virion-associated protein that is required for HIV-1 replication in macrophages and regulates viral gene expression in T cells [24].
• A mouse T-lymphosarcoma cell line stably infected with mouse mammary tumor virus (MMTV) was used as the parent line for a genetic analysis of two glucocorticoid hormone responses, hormone-induced cytolysis and stimulation of viral gene expression [25].

Associations of Genes, Viral with chemical compounds

• Viral gene expression was increased by the addition of dexamethasone [26].
• Transcriptional control of viral gene therapy by cisplatin [27].
• Viral gene delivery selectively restores feeding and prevents lethality of dopamine-deficient mice [28].
• This viral gene product phosphorylates the prodrug ganciclovir to form a nucleoside analog that inhibits DNA synthesis [29].
• These results demonstrate that the recruitment of CBP, SWI/SNF, and TRAP/Mediator complexes by RTA is the principal mechanism to direct well-controlled viral gene expression and thereby viral lytic reactivation [30].

Gene context of Genes, Viral

• An association between viral genes and human oncogenic alterations: the adenovirus E1A induces the Ewing tumor fusion transcript EWS-FLI1 [31].
• The Epstein-Barr virus-immortalizing protein EBNA2 activates both cellular and viral gene expression by targeting CBF1 and mimicking NotchIC [32].
• Correction of the retinal dystrophy phenotype of the RCS rat by viral gene transfer of Mertk [33].
• The viral transactivator Tax activates the VEGF promoter, linking the induction of angiogenesis to viral gene expression [34].
• Mitotic repression of transcription of various cellular and viral gene promoters by RNA polymerase II can be reproduced in vitro either with extracts prepared from cells arrested at mitosis with the microtubule polymerization inhibitor nocodazole or with nuclear extracts prepared from asynchronous cells and the mitotic protein kinase cdc2/cyclin B [35].

Analytical, diagnostic and therapeutic context of Genes, Viral

• By use of naturally occurring viral reassortants and recombinant viruses generated by reverse genetic techniques, we investigated the viral genes associated with the TNF-alpha response [36].
• Consequently, E4 viral gene products present in DeltaE1 or DeltaE1 DeltaE3 Ad vectors induce G2 growth arrest, which may pose new and unintended consequences for human gene transfer and gene therapy [37].
• Results from restriction endonuclease mapping of c-myc and from analysis of heteroduplexes between the DNAs of the cellular and viral genes show that c-myc is homologous to 1,500 nucleotides in v-myc DNA [38].
• As shown by Northern blot analysis and immunohistochemical staining, leflunomide neither interferes with transcription of immediate early or late viral genes, nor with expression of corresponding proteins [39].
• Co-culture of EBV-positive BL cells with CD40-ligand-transfected L cells induced up-regulation of CD54 and CD80 but did not affect the expression of viral genes [40].

References