The cellular transcription factor USF cooperates with varicella-zoster virus immediate-early protein 62 to symmetrically activate a bidirectional viral promoter

1994 ◽  
Vol 14 (10) ◽  
pp. 6896-6906 ◽  
Author(s):  
J L Meier ◽  
X Luo ◽  
M Sawadogo ◽  
S E Straus
Keyword(s):  
Dna Binding ◽  
Varicella Zoster Virus ◽  
Dominant Negative ◽  
Immediate Early ◽  
Activation Process ◽  
Viral Promoter ◽  
Varicella Zoster ◽  
Cellular Transcription Factor ◽  
Early Protein ◽  
Target Promoters

The mechanisms governing the function of cellular USF and herpesvirus immediate-early transcription factors are subjects of considerable interest. In this regard, we identified a novel form of coordinate gene regulation involving a cooperative interplay between cellular USF and the varicella-zoster virus immediate-early protein 62 (IE 62). A single USF-binding site defines the potential level of IE 62-dependent activation of a bidirectional viral early promoter of the DNA polymerase and major DNA-binding protein genes. We also report a dominant negative USF-2 mutant lacking the DNA-binding domain that permits the delineation of the biological role of both USF-1 and USF-2 in this activation process. The symmetrical stimulation of the bidirectional viral promoter by IE 62 is achieved at concentrations of USF-1 (43 kDa) or USF-2 (44 kDa) already existing in cells. Our observations support the notion that cellular USF can intervene in and possibly target promoters for activation by a herpesvirus immediate-early protein.

scholarly journals The cellular transcription factor USF cooperates with varicella-zoster virus immediate-early protein 62 to symmetrically activate a bidirectional viral promoter.

1994 ◽  
Vol 14 (10) ◽  
pp. 6896-6906 ◽  
Author(s):  
J L Meier ◽  
X Luo ◽  
M Sawadogo ◽  
S E Straus
Keyword(s):  
Dna Binding ◽  
Varicella Zoster Virus ◽  
Dominant Negative ◽  
Immediate Early ◽  
Activation Process ◽  
Viral Promoter ◽  
Varicella Zoster ◽  
Cellular Transcription Factor ◽  
Early Protein ◽  
Target Promoters

The mechanisms governing the function of cellular USF and herpesvirus immediate-early transcription factors are subjects of considerable interest. In this regard, we identified a novel form of coordinate gene regulation involving a cooperative interplay between cellular USF and the varicella-zoster virus immediate-early protein 62 (IE 62). A single USF-binding site defines the potential level of IE 62-dependent activation of a bidirectional viral early promoter of the DNA polymerase and major DNA-binding protein genes. We also report a dominant negative USF-2 mutant lacking the DNA-binding domain that permits the delineation of the biological role of both USF-1 and USF-2 in this activation process. The symmetrical stimulation of the bidirectional viral promoter by IE 62 is achieved at concentrations of USF-1 (43 kDa) or USF-2 (44 kDa) already existing in cells. Our observations support the notion that cellular USF can intervene in and possibly target promoters for activation by a herpesvirus immediate-early protein.

scholarly journals Identification of phosphorylated residues on varicella-zoster virus immediate-early protein ORF63

2010 ◽  
Vol 91 (5) ◽  
pp. 1133-1137 ◽  
Author(s):  
N. H. Mueller ◽  
M. S. Walters ◽  
R. A. Marcus ◽  
L. L. Graf ◽  
J. Prenni ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Immediate Early ◽  
Varicella Zoster ◽  
Early Protein

scholarly journals Mutational analysis of varicella-zoster virus (VZV) immediate early protein (IE62) subdomains and their importance in viral replication

Virology ◽  
2016 ◽  
Vol 492 ◽  
pp. 82-91 ◽  
Author(s):  
Mohamed I. Khalil ◽  
Xibing Che ◽  
Phillip Sung ◽  
Marvin H. Sommer ◽  
John Hay ◽  
...  
Keyword(s):  
Viral Replication ◽  
Varicella Zoster Virus ◽  
Mutational Analysis ◽  
Immediate Early ◽  
Varicella Zoster ◽  
Early Protein

scholarly journals Antibody to Varicella-Zoster Virus Immediate-Early Protein 62 Augments Allodynia in Zoster via Brain-Derived Neurotrophic Factor

2009 ◽  
Vol 84 (3) ◽  
pp. 1616-1624 ◽  
Author(s):  
Yuka Hama ◽  
Kimiyasu Shiraki ◽  
Yoshihiro Yoshida ◽  
Atsushi Maruyama ◽  
Makoto Yasuda ◽  
...  
Keyword(s):  
Varicella Zoster Virus ◽  
Nerve Injury ◽  
Neurotrophic Factor ◽  
Mechanical Allodynia ◽  
Brain Derived Neurotrophic Factor ◽  
Cross Reactivity ◽  
Immediate Early ◽  
Morphological Development ◽  
Varicella Zoster ◽  
Early Protein

ABSTRACT Varicella-zoster virus (VZV) expresses immediate-early protein 62 (IE62), and zoster is associated with neuropathic pain. Brain-derived neurotrophic factor (BDNF) is involved in the neuronal mechanism underlying pain hypersensitivity. Zoster is associated with prodrome and the robust production of booster antibody to VZV. We hypothesized that the intrathecal production of antibody to IE62 cross-reacting with BDNF and the nerve injury by skin lesions may augment allodynia in zoster by enhancing BDNF activity. One of three monoclonal antibodies against the 268-556 peptide of IE62 recognized BDNF. Immunological cross-reactivity between IE62 and BDNF and the effects of anti-IE62 monoclonal antibody (anti-IE62 MAb) cross-reactivity with BDNF on BDNF activity in cultured neurons were examined. Anti-IE62 MAb and anti-BDNF MAbs recognized the 414-429 peptide of IE62 and the BDNF dimer. Anti-IE62 MAb significantly augmented BDNF-related transcription in neurons and the morphological development of spinal dorsal horn neurons. Sera from patients recognized IE62 and BDNF and enhanced BDNF activity in neurons. The effect of anti-IE62 antibody on mechanical allodynia was characterized by the threshold of allodynia using von Frey filaments in a spinal nerve injury (SNI) in mice. The administration of anti-IE62 MAb to or immunization with cross-reacting IE62 protein to mice significantly enhanced mechanical allodynia on the side with SNI but not on the uninjured side. Anti-IE62 antibody augmented BDNF activity in neurons and allodynia in mice with SNI. The intrathecal production of anti-IE62 antibody augmenting BDNF activity and peripheral nerve injury by zoster may participate in the pathogenesis of allodynia in zoster.

The Varicella-Zoster virus immediate early protein, IE62, can positively regulate its cognate promoter

Virology ◽  
1992 ◽  
Vol 191 (1) ◽  
pp. 346-354 ◽  
Author(s):  
L.P. Perera ◽  
J.D. Mosca ◽  
M. Sadeghi-Zadeh ◽  
W.T. Ruyechan ◽  
J. Hay
Keyword(s):  
Varicella Zoster Virus ◽  
Immediate Early ◽  
Varicella Zoster ◽  
Early Protein

scholarly journals Phosphorylation of the Nuclear Form of Varicella-Zoster Virus Immediate-Early Protein 63 by Casein Kinase II at Serine 186

2009 ◽  
Vol 83 (23) ◽  
pp. 12094-12100 ◽  
Author(s):  
Niklaus H. Mueller ◽  
Laurie L. Graf ◽  
David Orlicky ◽  
Don Gilden ◽  
Randall J. Cohrs
Keyword(s):  
Monoclonal Antibody ◽  
Varicella Zoster Virus ◽  
Casein Kinase Ii ◽  
Casein Kinase ◽  
Antibody Binding ◽  
Immediate Early ◽  
Productive Infection ◽  
Varicella Zoster ◽  
Recombinant Monoclonal Antibody ◽  
Early Protein

ABSTRACT Varicella-zoster virus (VZV) open reading frame (ORF) 63 is abundantly transcribed in latently infected human ganglia and encodes a 278-amino-acid protein, IE63, with immediate-early kinetics. IE63 is expressed in the cytoplasm of neurons during VZV latency and in both the cytoplasm and the nucleus during productive infection; however, the mechanism(s) involved in IE63 nuclear import and retention has remained unclear. We constructed and identified a recombinant monoclonal antibody to detect a posttranslationally modified form of IE63. Analysis of a series of IE63 truncation and substitution mutants showed that amino acids 186 to 195 are required for antibody binding. Synthetic peptides corresponding to this region identified IE63 S186 as a target for casein kinase II phosphorylation. In addition, acidic charges supplied by E194 and E195 were required for antibody binding. Immunofluorescence analysis of VZV-infected MeWo cells using the recombinant monoclonal antibody detected IE63 exclusively in the nuclei of infected cells, indicating that casein kinase II phosphorylation of S186 occurs in the nucleus and possibly identifying an initial molecular event operative in VZV reactivation.

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