scholarly journals Induction of RANTES/CCL5 by herpes simplex virus is regulated by nuclear factor κB and interferon regulatory factor 3

2003 ◽  
Vol 84 (9) ◽  
pp. 2491-2495 ◽  
Author(s):  
Jesper Melchjorsen ◽  
Søren R. Paludan
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Nuclear Factor Κb ◽  
Interferon Regulatory Factor ◽  
Nuclear Factor ◽  
Regulatory Factor ◽  
Interferon Regulatory Factor 3 ◽  
Simplex Virus

scholarly journals Involvement of HVEM receptor in activation of nuclear factor κB by herpes simplex virus 1 glycoprotein D

2008 ◽  
Vol 10 (11) ◽  
pp. 2297-2311 ◽  
Author(s):  
Maria Teresa Sciortino ◽  
Maria Antonietta Medici ◽  
Francesca Marino-Merlo ◽  
Daniela Zaccaria ◽  
Maria Giuffrè-Cuculletto ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Glycoprotein D ◽  
Herpes Simplex Virus 1 ◽  
Simplex Virus

scholarly journals Use of Differential Display Reverse Transcription-PCR To Reveal Cellular Changes during Stimuli That Result in Herpes Simplex Virus Type 1 Reactivation from Latency: Upregulation of Immediate-Early Cellular Response Genes TIS7, Interferon, and Interferon Regulatory Factor-1

1998 ◽  
Vol 72 (2) ◽  
pp. 1252-1261 ◽  
Author(s):  
Ruth Tal-Singer ◽  
Wawrzyniec Podrzucki ◽  
Todd M. Lasner ◽  
Aikaterini Skokotas ◽  
Jeffry J. Leary ◽  
...  
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Interferon Regulatory Factor ◽  
Regulatory Factor ◽  
Reverse Transcription Pcr ◽  
Interferon Regulatory Factor 1 ◽  
Cellular Factors ◽  
Differential Display Reverse Transcription ◽  
Simplex Virus

ABSTRACT The detailed mechanism which governs the choice between herpes simplex virus (HSV) latency and reactivation remains to be elucidated. It is probable that altered expression of cellular factors in sensory neurons leads to induction of HSV gene expression resulting in reactivation. As an approach to identify novel cellular genes which are activated or repressed by stimuli that reactivate HSV from latency and hence may play a role in viral reactivation, RNA from explanted trigeminal ganglia (TG) was analyzed by differential display reverse transcription-PCR (DDRT-PCR). Nearly 50 cDNAs whose mRNA level was modified by the stress of explantation were isolated and sequenced. We present a listing of a spectrum of altered RNAs, including both known and unknown sequences. Five of those differentially displayed transcripts were identified as interferon-related murine TIS7 mRNA. These results were confirmed in both infected and uninfected ganglia by quantitative RNase protection assay and immunostaining. Alpha and beta interferons and interferon regulatory factor-1 (IRF-1) were also induced by explantation. In addition, we have identified sequences that correspond to IRF-1 consensus binding sites in both HSV type 1 origins of replication. Our findings suggest that physiological pathways that include these cellular factors may be involved in modulating HSV reactivation.

Resveratrol suppresses nuclear factor-κB in herpes simplex virus infected cells

2006 ◽  
Vol 72 (3) ◽  
pp. 242-251 ◽  
Author(s):  
Seth A. Faith ◽  
Thomas J. Sweet ◽  
Erin Bailey ◽  
Tristan Booth ◽  
John J. Docherty
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Infected Cells ◽  
Simplex Virus

scholarly journals Control of Herpes Simplex Virus Replication Is Mediated through an Interferon Regulatory Factor 3-Dependent Pathway

2009 ◽  
Vol 83 (23) ◽  
pp. 12399-12406 ◽  
Author(s):  
Vineet D. Menachery ◽  
David A. Leib
Keyword(s):  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Virus Replication ◽  
Early Recognition ◽  
Critical Role ◽  
Type I ◽  
Type I Ifn ◽  
Regulatory Factor ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT The type I interferon (IFN) cascade is critical in controlling viral replication and pathogenesis. Recognition pathways triggered by viral infection rapidly induce the type I IFN cascade, often in an IFN regulatory factor 3 (IRF-3)-dependent fashion. This dependence predicts that loss of IRF-3 would render early recognition pathways inoperative and thereby impact virus replication, but this has not been observed previously with herpes simplex virus type 1 (HSV-1) in vitro. In this study, HSV-1-infected IRF-3−/− bone marrow-derived dendritic cells (BMDCs) and macrophages supported increased HSV replication compared to control cells. In addition, IRF-3-deficient BMDCs exhibited delayed type I IFN synthesis compared to control cells. However, while IFN pretreatment of IRF-3−/− BMDCs resulted in reduced virus titers, a far greater reduction was seen after IFN treatment of wild-type cells. This suggests that even in the presence of exogenously supplied IFN, IRF-3−/− BMDCs are inherently defective in the control of HSV-1 replication. Together, these results demonstrate a critical role for IRF-3-mediated pathways in controlling HSV-1 replication in cells of the murine immune system.

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