Proteins and cis-acting elements associated with transactivation of the varicella-zoster virus (VZV) immediate-early gene 62 promoter by VZV open reading frame 10 protein.

1995 ◽  
Vol 69 (8) ◽  
pp. 4693-4701 ◽  
Author(s):  
H Moriuchi ◽  
M Moriuchi ◽  
J I Cohen
1998 ◽  
Vol 72 (1) ◽  
pp. 857-861 ◽  
Author(s):  
Adrian Whitehouse ◽  
Matthew Cooper ◽  
David M. Meredith

ABSTRACT The herpesvirus saimiri (HVS) immediate-early gene product encoded by open reading frame (ORF) 57 shares limited amino acid homology with HSV-1 ICP27 and Epstein-Barr virus BMLF1, both regulatory proteins. The ORF 57 gene has been proposed to be spliced based on the genome sequence, and here we confirm the intron-exon structure of the gene. We also demonstrate that a cDNA construct of the ORF 57 gene product represses the transactivating capability of the ORF 50a gene product (which is produced from a spliced transcript), but activates that of ORF 50b (an unspliced transcript). Further analyses with cotransfection experiments show that ORF 57 can either activate or repress expression from a range of both early and late HVS promoters, depending on the target gene. These results indicate that repression of gene expression mediated by the ORF 57 gene product is dependent on the presence of an intron within the target gene encoding region. Furthermore, Northern blot analysis demonstrates that the levels of mRNA transcribed from genes not containing an intron are not significantly affected in the presence of the ORF 57 gene product. This suggests that it regulates gene expression through a posttranscriptional mechanism.


1990 ◽  
Vol 71 (4) ◽  
pp. 897-906 ◽  
Author(s):  
T. A. McKee ◽  
G. H. Disney ◽  
R. D. Everett ◽  
C. M. Preston

2006 ◽  
Vol 80 (7) ◽  
pp. 3238-3248 ◽  
Author(s):  
Xibing Che ◽  
Leigh Zerboni ◽  
Marvin H. Sommer ◽  
Ann M. Arvin

ABSTRACT The open reading frame 10 (ORF10) of varicella-zoster virus (VZV) encodes a tegument protein that enhances transactivation of VZV genes and has homology to herpes simplex virus type 1 (HSV-1) VP16. While VP16 is essential for HSV replication, ORF10 is dispensable for vaccine OKA (VOKA) growth in vitro. We used parent OKA (POKA) cosmids to delete ORF10, producing POKAΔ10; point mutations that disrupted the acidic activation domain and the putative motif for binding human cellular factor 1 (HCF-1) in ORF10 protein yielded POKA10-Phe28Ala, POKA10-Phe28Ser, and POKA10-mHCF viruses. Deleting ORF10 or mutating these two functional domains had no effect on VZV replication, immediate-early gene transcription, or virion assembly in vitro. However, deleting ORF10 reduced viral titers and the extent of cutaneous lesions significantly in SCIDhu skin xenografts in vivo compared to POKA. Epidermal cells infected with POKAΔ10 had significantly fewer DNA-containing nucleocapsids and complete virions compared to POKA; extensive aggregates of intracytoplasmic viral particles were also observed. Altering the activation or the putative HCF-1 domains of ORF10 protein had no consequences for VZV replication in vivo. Thus, the decreased pathogenic potential of POKAΔ10 in skin could not be attributed to absence of these ORF10 protein functions. In contrast to skin cells, deleting ORF10 did not impair VZV T-cell tropism in vivo, as assessed by infectious virus yields. We conclude that ORF10 protein is required for efficient VZV virion assembly and is a specific determinant of VZV virulence in epidermal and dermal cells in vivo.


Virology ◽  
1990 ◽  
Vol 179 (1) ◽  
pp. 365-377 ◽  
Author(s):  
Čestmǐr Vlček ◽  
Zbynek Kozmǐk ◽  
Václav Paces ◽  
Sabine Schirm ◽  
Martin Schwyzerv

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