Herpes Simplex Virus Latency and Immediate Early Gene Repression by the Cellular Octamer-Binding Protein Oct-2

1994 ◽  
pp. 238-252 ◽  
Author(s):  
David S. Latchman
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Binding Protein ◽  
Immediate Early Gene ◽  
Early Gene ◽  
Gene Repression ◽  
Immediate Early ◽  
Virus Latency ◽  
Simplex Virus

scholarly journals Herpes Simplex Virus Downregulates Secretory Leukocyte Protease Inhibitor: a Novel Immune Evasion Mechanism

2008 ◽  
Vol 82 (19) ◽  
pp. 9337-9344 ◽  
Author(s):  
Esra Fakioglu ◽  
Sarah S. Wilson ◽  
Pedro M. M. Mesquita ◽  
Ehsan Hazrati ◽  
Natalia Cheshenko ◽  
...  
Keyword(s):  
Gene Expression ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Protease Inhibitor ◽  
Immediate Early Gene ◽  
Secretory Leukocyte Protease Inhibitor ◽  
Early Gene ◽  
Immediate Early ◽  
Early Gene Expression ◽  
Simplex Virus

ABSTRACT Secretory leukocyte protease inhibitor (SLPI), an anti-inflammatory mediator of mucosal immunity, inhibits human immunodeficiency virus (HIV) and herpes simplex virus (HSV) in cell culture. Epidemiological studies demonstrate that higher concentrations of SLPI in mucosal secretions are associated with a reduced risk of HIV transmission. The current studies were designed to test the hypothesis that HSV triggers a loss of SLPI to evade innate immunity and that this response may contribute to the increased risk of HIV infection in the setting of HSV infection. Exposure of human cervical epithelial cells to HSV-1 or HSV-2, but not HIV or vesicular stomatitis virus, triggered a significant and sustained reduction in SLPI levels. The reduction persisted when cells were infected in the presence of acyclovir but not following infection with UV-inactivated virus, indicating that viral gene expression, but not replication, is required. Reverse transcriptase PCR studies demonstrated that the loss of SLPI is mediated by downregulation of gene expression. SLPI downregulation was associated with activation of NF-κB signaling pathways and upregulation of proinflammatory cytokines, consistent with the known inhibitor effects of SLPI on NF-κB pathways. The downregulation mapped to viral early-gene expression, as variants impaired in expression of the ICP4 or ICP0 immediate-early gene failed to downregulate SLPI or activate NF-κB. Together, these results identify a novel role for HSV immediate-early-gene expression in regulating mucosal immune responses.

scholarly journals Herpes Simplex Virus Latency-Associated Transcript Encodes a Protein Which Greatly Enhances Virus Growth, Can Compensate for Deficiencies in Immediate-Early Gene Expression, and Is Likely To Function during Reactivation from Virus Latency

1999 ◽  
Vol 73 (8) ◽  
pp. 6618-6625 ◽  
Author(s):  
S. K. Thomas ◽  
G. Gough ◽  
D. S. Latchman ◽  
R. S. ◽  
Coffin
Keyword(s):  
Gene Expression ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Early Gene ◽  
Immediate Early ◽  
Productive Infection ◽  
Wild Type Virus ◽  
Virus Growth ◽  
Virus Latency ◽  
Simplex Virus

ABSTRACT Herpes simplex virus types 1 and 2 (HSV1 and HSV2) enter and reactivate from latency in sensory neurons, although the events governing these processes are little understood. During latency, only the latency-associated transcripts (LATs) are produced. However, although the LAT RNAs were described ≈10 years ago, their function remains ambiguous. Mutations affecting the LATs have minimal effects other than a small reduction in establishment of and reactivation from latency in some cases. Mutations in putative LAT-contained open reading frames (ORFs) have so far shown no effect. The LATs consist of a large species from which smaller (≈2 kb), nuclear, nonlinear LATs which are abundant during latency are spliced. Thus, translation of ORFs in these smaller LATs would not usually be expected to be possible, and if expressed at all, their expression might be tightly regulated. Here we show that deregulated expression of the largest HSV1 2-kb LAT-contained ORF in various cells of neuronal and nonneuronal origin greatly enhances virus growth in a manner specific to HSV1—the HSV1 LAT ORF has no effect on the growth of HSV2. Similar results of enhanced growth were found when the HSV1 LAT ORF was constitutively expressed from within the HSV1 genome. The mechanism of LAT ORF action was strongly suggested to be by substituting for deficiencies in immediate-early (IE) gene expression (particularly ICP0), because deregulated LAT ORF expression, as well as enhancing wild-type virus growth, was also found to allow efficient growth of viruses with mutations in ICP0 or VMW65. Such viruses otherwise exhibit considerable growth defects. IE gene expression deficiencies are often the block to productive infection in nonpermissive cells and are also evident during latency. These results, which we show to be protein- rather than RNA-mediated effects, strongly suggest a function of the tightly regulated expression of a LAT ORF-encoded protein in the reactivation from HSV latency.

Lupeol impairs herpes simplex virus type 1 replication by inhibiting the promoter activity of the viral immediate early gene α0

2021 ◽  
Vol 65 (03) ◽  
pp. 254-263
Author(s):  
Ju Ye ◽  
Zhaoyang Wang ◽  
Jiaoyan Jia ◽  
Feng Li ◽  
Yiliang Wang ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Type ◽  
Herpes Simplex Virus Type ◽  
Promoter Activity ◽  
Immediate Early Gene ◽  
Early Gene ◽  
Immediate Early ◽  
Simplex Virus

scholarly journals Properties of a herpes simplex virus multiple immediate-early gene-deleted recombinant as a vaccine vector

Virology ◽  
2007 ◽  
Vol 357 (2) ◽  
pp. 186-198 ◽  
Author(s):  
Daisuke Watanabe ◽  
Mark A. Brockman ◽  
Thumbi Ndung'u ◽  
Lydia Mathews ◽  
William T. Lucas ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Immediate Early Gene ◽  
Vaccine Vector ◽  
Early Gene ◽  
Immediate Early ◽  
Simplex Virus
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