Disease relevance of Virus Activation

• The procedure proved to be particularly useful in studies of murine leukemia viruses, because it allowed virus induction and Fv-1 gene-typing tests to the done on biopsy tissue from adult animals [1].
• Studies on virus induction by 5-bromodeoxyuridine in nonproducer murine sarcoma virus-transformed 3T3 cells [2].
• We have examined the ability of phenol and the 19 isomers of chlorophenol to induce DNA damage using the Microscreen prophage-induction assay in Escherichia coli [3].
• We combined hydroxyurea, a cytostatic drug that inhibits cell activation and proliferation, with two drugs that inhibit HIV (didanosine and indinavir), to block the "cell activation-virus production-pathogenesis" cycle [4].
• The pattern of virus activation in the ganglion tissue was similar irrespective of whether the explants were cultured in the presence or absence of 5-bromo-2'-deoxyuridine [5].

High impact information on Virus Activation

• In this paper, we investigate DNA bending induced by proteins required for virus induction of the human interferon-beta (IFN beta) gene [6].
• Mutations that interfere with binding of either protein decrease the level of virus induction, and activation of the gene can be blocked by either NF-kappa B or HMG I(Y) antisense RNA [7].
• A detailed comparison between Mov-1 and Mov-13 mice demonstrated that the time of virus activation is different [8].
• PRDI-BF1 blocks virus induction of the intact beta-IFN gene promoter and of synthetic promoters containing multiple PRDI sites [9].
• Virus induction is amplified by 5-bromo-2'-deoxyuridine (BrdU) treatment [10].

Biological context of Virus Activation

• An ATF/CREB binding site is required for virus induction of the human interferon beta gene [corrected] [11].
• To investigate whether virus activation occurs during lymphoid cell differentiation, hematopoietic stem cells carrying the endogenous Mov-1 genome were transplanted to sublethally irradiated BALB/c mice [12].
• Complexity and abundance of murine leukemia virus-related nuclear and messenger RNA sequences in mouse embryo cell lines which are differentially sensitive to carcinogen-induced virus activation [13].
• The influence of the major histocompatibility complex of the mouse (H-2 complex) on the antibody response against murine leukemia virus (MuLV) was investigated after 3 different ways of virus presentation (milk transmission of virus, spontaneous virus activation, and immunization with inactivated virus) [14].
• Although sera from a number of squirrel monkeys contained antibody to SMRV p35, the possibility that this latter reactivity was due to endogenous virus activation rather than horizontal transmission cannot be ruled out [15].

Anatomical context of Virus Activation

• Some of the endogenous env sequences appear to be closely linked to genes determining leukemia virus induction and to genes involved in the immune response, such as the heavy and light chains of the immunoglobulin molecules or allotypic determinants on B and T lymphocytes [16].
• Normal melanocytes were found to secrete both IFN-alpha and IFN-beta after virus induction [17].
• Double-labeling with specific monoclonal antibodies to T and B lymphocytes confirmed that the entire populations of these two cell types produce IFN-alpha, both constitutively and after virus induction [18].
• Partially synchronized cells cultured with aminoethylcysteine (AEC), parafluorophenylalanine (PFA), or valinol, and subsequently induced with either 5-iododeoxyuridine (IUdR), cycloheximide, or histidinol, showed inhibition of virus activation [19].

Associations of Virus Activation with chemical compounds

• Enhancement of 5-iododeoxyuridine-induced endogenous C-type virus activation by polycyclic hydrocarbons: apparent lack of parallelism between enhancement and carcinogenicity [20].
• These findings suggest that multiple injections of streptozotocin induce, in susceptible hosts, the triad of direct beta cell cytotoxicity, virus induction within beta cells, and cell-mediated autoimmune reaction [21].
• Cell cycle-specific enhancement of type C virus activation by sodium n-butyrate [22].
• During the time cells were exposed to these compounds, there was little inhibition of [3H]uridine incorporation into total cellular RNA or polyadenylic acid cytoplasmic messenger RNA, suggesting that inhibition of proteolysis, and not RNA transcription, was responsible for blocking virus induction [23].
• The high frequency of induction by 5-azacytidine, relative to other nucleoside analogs, and the absence of induction by other mutagens further indicate that endogenous virus induction occurs via nonmutagenic mechanisms and that some mutagens may also affect regulatory functions independent of their mutagenic action [24].

Gene context of Virus Activation

• Proteins containing only this domain can function as a dominant-negative inhibitor of PRDI-BF1 repression, and can significantly increase the IFN-beta promoter activity after virus induction [25].
• Virus activation was caused by a sensitization of TNF-R1 toward endogenously produced tumor necrosis factor alpha (TNF-alpha) [26].
• Here we report that V and W proteins also block virus activation of the beta interferon (IFN-beta) promoter and the IFN regulatory factor 3 (IRF3)-responsive IFN-stimulated gene 54 promoter [27].
• Treatment with IFN-alpha prior to virus induction did not increase further CAT activity [28].
• Mutations in PRDIV that decrease the affinity of one member of this family (ATF-2/CRE-BP1) decrease the level of virus induction in vivo [11].

References