Detection of Human Serum Antibodies to the BFRF3 Epstein-Barr Virus Capsid Component by Means of a DNA-Binding Assay

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 disrupt viral latency; expression of the BZLF1 gene is both necessary and sufficient for triggering the viral lytic cascade. We have previously shown that Zta can activate its own promoter (Zp), through binding to two Zta recognition sequences (ZIIIA and ZIIIB). Here we describe mutant Zta proteins that do not bind DNA (referred to as Zta DNA-binding mutants [Zdbm]) but retain the ability to transactivate Zp. Consistent with the inability of these mutants to bind DNA, transactivation of Zp by Zdbm is not dependent on the Zta recognition sequences. Instead, transactivation by Zdbm is dependent upon promoter elements that bind cellular factors. An examination of other viral and cellular promoters identified promoters that are weakly responsive or unresponsive to Zdbm. An analysis of a panel of artificial promoters containing one copy of various promoter elements demonstrated a specificity for Zdbm activation that is distinct from that of Zta. These results suggest that non-DNA-binding forms of some transactivators retain the ability to transactivate specific target promoters without direct binding to DNA.

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Chemokine CCL27 is a novel plasma biomarker for identification the nasopharyngeal carcinoma patients from the Epstein-Barr virus capsid antigen-specific IgA seropositive population

BMC Cancer ◽

10.1186/s12885-017-3718-2 ◽

2018 ◽

Vol 18 (1) ◽

Cited By ~ 4

Author(s):

Min-jie Mao ◽

Ning Xue ◽

Xue-ping Wang ◽

Pei-dong Chi ◽

Yi-jun Liu ◽

...

Keyword(s):

Nasopharyngeal Carcinoma ◽

Epstein Barr Virus ◽

Plasma Biomarker ◽

Virus Capsid ◽

Barr Virus ◽

Epstein Barr ◽

Virus Capsid Antigen

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Epstein–Barr virus induces a distinct form of DNA-bound STAT1 compared with that found in interferon-stimulated B lymphocytes

Journal of General Virology ◽

10.1099/vir.0.82741-0 ◽

2007 ◽

Vol 88 (7) ◽

pp. 1876-1886 ◽

Cited By ~ 13

Author(s):

James McLaren ◽

Martin Rowe ◽

Paul Brennan

Keyword(s):

Dna Binding ◽

Epstein Barr Virus ◽

Lymphoblastoid Cell Lines ◽

Distinct Form ◽

Post Translational Modifications ◽

Constitutive Activation ◽

Barr Virus ◽

Molecular Identity ◽

Infected Cells ◽

Epstein Barr

Since ‘constitutive activation’ of STAT1 was first described in Epstein–Barr virus (EBV)-immortalized lymphoblastoid cell lines (LCLs), there has been controversy regarding the molecular identity of the STAT1 DNA-binding complex found in these cells. The post-translational modifications of STAT1 in LCLs have been analysed and an LMP1-induced STAT1 DNA-binding complex, different from that generated by alpha interferon (IFN) stimulation and not involving tyrosine phosphorylation, is demonstrated. STAT1 is serine-phosphorylated downstream of PI3K and MEK in LCLs and this modification restricts IFN-stimulated STAT1–DNA binding. These data suggest that EBV induces a distinct form of DNA-bound STAT1 in virus-infected cells.

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