Epstein-Barr virus induction by a serum factor I. Induction and cooperation with additional inducers

Bauer, Georg; Höfler, Petra; Hausen, Harald zur

doi:10.1016/0042-6822(82)90128-3

Cited by 76 publications

(50 citation statements)

References 12 publications

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“…Yamamoto et aL (1980) have described cooperativity for the combined action of TPA plus 5'-iodo-2'-deoxyuridine (IUdR) and TPA plus n-BA, whereas Tovey et al (1978) did not observe cooperation between TPA and IUdR but did find cooperation with IUdR and antibody to IgM. We have shown recently that a serum factor can efficiently cooperate with TPA, IUdR, n-BA and anti-IgM (Bauer et al, 1982a).…”

Section: Introductionmentioning

confidence: 99%

“…The serum was activated in the same way as the factor. Fifty ~tl of activated serum per ml of assay mixture contained saturating amounts of active serum factor (Bauer et al, 1982a).…”

Section: Ebv-genome-positive Cell Linesmentioning

confidence: 99%

“…It has been noted before that combined application of inducers may lead to much higher values of induced cells than the sum of cells induced by application of individual inducers (Tovey et al, 1978;Lenoir, 1979;Yamamoto et al, 1980;Ito et al, 1981 ;Bauer et al, 1982a). Lenoir (1979) as well as Ito et al (1981) have reported cooperation for the action of 12-Otetradecanoylphorbol 13-acetate (TPA) plus n-butyric acid (n-BA).…”

Section: Introductionmentioning

confidence: 99%

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Quantitative Analysis of the Cooperative Effect between Inducers of Epstein--Barr Virus Antigen Synthesis

Bauer

1983

Journal of General Virology

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Section: Introductionmentioning

confidence: 99%

“…The serum was activated in the same way as the factor. Fifty ~tl of activated serum per ml of assay mixture contained saturating amounts of active serum factor (Bauer et al, 1982a).…”

Section: Ebv-genome-positive Cell Linesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Quantitative Analysis of the Cooperative Effect between Inducers of Epstein--Barr Virus Antigen Synthesis

Bauer

1983

Journal of General Virology

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“…Propagation of EBV from host to host is dependent upon the activation of an estimated 100 or more viral genes, culminating in the production of infectious virions (2,4,9,27). While these genes remain quiescent during latency, a switch in the genetic program leading to the expression of viral replication associated genes can be accomplished in vitro by treatment of latently infected B lymphocytes with various reagents, including phorbol esters, butyrate, ionophore, and anti-immunoglobulin (2,28,37,46,48,51).…”

mentioning

confidence: 99%

DNA-binding-defective mutants of the Epstein-Barr virus lytic switch activator Zta transactivate with altered specificities.

et al. 1994

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The Epstein-Barr virus BRLF1 and BZLF1 genes are the first viral genes transcribed upon induction of the viral lytic cycle. The protein products of both genes (referred to here as Rta and Zta, respectively) activate expression of other viral genes, thereby initiating the lytic cascade. Among the viral antigens expressed upon induction of the lytic cycle, however, Zta is unique in its ability to Epstein-Barr virus (EBV) is a lymphotropic human herpesvirus that latently infects B lymphocytes, resulting in a concomitant growth transformation of the infected cell. Infection is closely associated with several human cancers, including nasopharyngeal carcinoma and African Burkitt's lymphoma, and also plays a role in several lymphoproliferative diseases in immunocompromised individuals (for a review, see reference 29). In vitro the transforming potential of EBV is evidenced by its ability to immortalize B lymphocytes to grow indefinitely in culture. Immortalization is achieved through the expression of a relatively small subset of EBV-encoded genes that serve to establish and maintain cellular transformation (for a review, see reference 45).Propagation of EBV from host to host is dependent upon the activation of an estimated 100 or more viral genes, culminating in the production of infectious virions (2, 4, 9, 27). While these genes remain quiescent during latency, a switch in the genetic program leading to the expression of viral replication associated genes can be accomplished in vitro by treatment of latently infected B lymphocytes with various reagents, including phorbol esters, butyrate, ionophore, and anti-immunoglobulin (2,28,37,46,48,51). Activation of the lytic cascade by treatment with anti-immunoglobulin results initially in the expression of two viral genes, BZLF1 and BRLF1, which exhibit similar induction kinetics (maximal mRNA levels are reached between 2 and 4 h postinduction) (14, 46). The protein products of both the BZLF1 (referred to here as Zta, but also called ZEBRA and EB1) and BRLF1 (Rta) genes have been shown to be transcriptional activators (8,10,12,25,26 speck@visar.wustl.edu.Expression of Zta and Rta leads to the activation of early genes and ultimately viral replication. Of all the viral transactivators examined, Zta is unique in that its expression alone can initiate the entire lytic cascade (10,11,40), and regulation of Zta expression appears to be central to regulating entry into the lytic cycle.We have previously identified multiple elements within the BZLF1 promoter (Zp) that play a role in regulating BZLF1 expression (15,16). Several of these elements bind cellular transcription factors that are responsive to phorbol ester stimulation (15). Zp also contains two Zta binding sites (ZIIIA and ZIIIB) that are important for autoactivation (16,33,49).Zta shares several structural similarities with other transcription factors. As described by Farrell et al. (12), Zta contains a basic region with homology to the DNA-binding domains of the AP-1 family of transcription factors (Fig. 1). In addi...

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“…Expression of a subset of the latter genes is sufficient to immortalize B cells and to maintain steady-state levels of the viral genome (31). Treatment of certain latently infected B-cell populations with reagents such as phorbol esters (5,17,64), Ca 2ϩ ionophores (15), sodium butyrate (26,38), and serum factors (2) or cross-linking of surface anti-immunoglobulin (12,21,50,53) leads to cellular differentiation and the concomitant induction of the rest of EBV's genes, followed by viral genome replication to higher copy number and production of infectious virus particles (28)(29)(30).…”

mentioning

confidence: 99%

Identification of a Novel Element Involved in Regulation of the Lytic Switch BZLF1 Gene Promoter of Epstein-Barr Virus

Kraus

Mirocha

Stephany

et al. 2001

J Virol

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Epstein-Barr virus (EBV) isEpstein-Barr virus (EBV) is a human herpesvirus that is estimated to infect up to 90% of the world's population (28,29). EBV infection is associated with several human diseases, including infectious mononucleosis, nasopharyngeal carcinoma, Burkitt's lymphoma, and, in immunosuppressed patients, B-cell and T-cell lymphomas (28,29). Thus, EBV is a serious pathogen and poses a significant threat to human health.Like other herpesviruses, primary infection with EBV is followed by a persistent infection of the human host. Oropharyngeal epithelium is thought to be the primary site of EBV infection and replication and of viral spread (28-30, 51), while B cells are the major site of persistent latency (28-31). Eleven of EBV's approximately 100 viral genes are expressed during latency. These include ones encoding the EBV-encoded nuclear antigens (EBNAs 1 to 6), the latent membrane proteins (LMPs 1 and 2), two EBV-encoded small nuclear RNAs, and the BamHIA transcripts (28, 29). Expression of a subset of the latter genes is sufficient to immortalize B cells and to maintain steady-state levels of the viral genome (31). Treatment of certain latently infected B-cell populations with reagents such as phorbol esters (5, 17, 64), Ca 2ϩ ionophores (15), sodium butyrate (26, 38), and serum factors (2) or cross-linking of surface anti-immunoglobulin (12, 21, 50, 53) leads to cellular differentiation and the concomitant induction of the rest of EBV's genes, followed by viral genome replication to higher copy number and production of infectious virus particles (28-30).Two immediate-early genes, BZLF1 and BRLF1, are the first to be expressed during induction of EBV out of latency (11,23,32,52). The protein products of both of these genes are strong transcriptional transactivators (9, 16). The product of the BZLF1 gene, referred to as Zta, ZEBRA, or EB1, plays a crucial role in the disruption of latency and initiation of the viral infectious cycle (10,11,41,46,52). Thus, regulation of Zta expression is critical to the state of EBV in cells.The transcriptional regulation of the BZLF1 promoter (also referred to as Zp) has been studied extensively. Zp exhibits very low basal activity and is readily activated by inducers of the viral infectious cycle. The cis-acting elements necessary both for basal activity and for response to exogenous inducers lie within the nucleotide (nt) Ϫ221 to ϩ12 region of the promoter relative to the transcriptional initiation site (12,17,18). These elements have been divided into three classes ( Fig. 1; also, see reference 36 and references therein). Four AT-rich elements, termed ZIA to ZID, are dispersed throughout the promoter. They can bind the transcription factors Sp1 and Sp3 (34) and myocyte enhancer factor 2D (37, 44). A second type of element, ZII, shares significant homology with the consensus CRE/AP-1 binding site (1,13,25,54). Finally, a region called ZIII contains multiple binding sites for the Zta protein itself (18). It has been proposed that activation of the BZLF1 gene oc...

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Epstein-Barr virus induction by a serum factor I. Induction and cooperation with additional inducers

Cited by 76 publications

References 12 publications

Quantitative Analysis of the Cooperative Effect between Inducers of Epstein--Barr Virus Antigen Synthesis

Quantitative Analysis of the Cooperative Effect between Inducers of Epstein--Barr Virus Antigen Synthesis

DNA-binding-defective mutants of the Epstein-Barr virus lytic switch activator Zta transactivate with altered specificities.

Identification of a Novel Element Involved in Regulation of the Lytic Switch BZLF1 Gene Promoter of Epstein-Barr Virus

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