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Alison M. Kesson, Nicholas J. C. King, Transcriptional Regulation of Major Histocompatibility Complex Class I by Flavivirus West Nile Is Dependent on NF-κB Activation, The Journal of Infectious Diseases, Volume 184, Issue 8, 15 October 2001, Pages 947–954, https://doi.org/10.1086/323603
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Abstract
Infection by the flavivirus West Nile (WNV) is associated with a virus-specific increase of major histocompatibility complex class I (MHC-I) molecules on the cell surface of diploid vertebrate cells. The increased MHC-I cell surface expression is functional and is associated with increased susceptibility to secondary WNV-immune and alloimmune cytotoxic T cells. WNV-induced up-regulation of cell surface MHC-I expression is associated with NF-κB activation and increased transcription of MHC-I mRNA. WNV infection increases luciferase activity of RAWa4 long terminal repeat (LTR) cells, which are transfected stably with a plasmid containing 2 NF-κB binding sites, the human immunodeficiency virus LTR linked to a luciferase reporter gene. The NF-κB—induced complexes are a p50/p65 heterodimer and another faster migrating species containing p50 homodimers. WNV-induced activation of NF-κB and the up-regulation of MHC-I were blocked by the protein kinase C inhibitor H-7 and salicylate, both of which block phosphorylation of inhibitor κB
- salicylates
- plasmids
- binding sites
- diploidy
- flavivirus
- genes, reporter
- hiv long terminal repeat
- luciferases
- major histocompatibility complex
- phosphorylation
- rna, messenger
- terminal repeat sequences
- t-lymphocytes, cytotoxic
- up-regulation (physiology)
- vertebrates
- west nile virus
- infections
- viruses
- transcriptional control
- protein kinase c inhibitor
- molecule
- complex
- alloimmunity