Suppression of NF-κB Activity: A Viral Immune Evasion Mechanism.
Liyao DengQiurui ZengMingshu WangAn-Chun ChengRenyong JiaShun ChenDekang ZhuMafeng LiuQiao YangYing WuXinxin ZhaoShaqiu ZhangYunya LiuYanling YuLing ZhangXiaoyue ChenPublished in: Viruses (2018)
Nuclear factor-κB (NF-κB) is an important transcription factor that induces the expression of antiviral genes and viral genes. NF-κB activation needs the activation of NF-κB upstream molecules, which include receptors, adaptor proteins, NF-κB (IκB) kinases (IKKs), IκBα, and NF-κB dimer p50/p65. To survive, viruses have evolved the capacity to utilize various strategies that inhibit NF-κB activity, including targeting receptors, adaptor proteins, IKKs, IκBα, and p50/p65. To inhibit NF-κB activation, viruses encode several specific NF-κB inhibitors, including NS3/4, 3C and 3C-like proteases, viral deubiquitinating enzymes (DUBs), phosphodegron-like (PDL) motifs, viral protein phosphatase (PPase)-binding proteins, and small hydrophobic (SH) proteins. Finally, we briefly describe the immune evasion mechanism of human immunodeficiency virus 1 (HIV-1) by inhibiting NF-κB activity in productive and latent infections. This paper reviews a viral mechanism of immune evasion that involves the suppression of NF-κB activation to provide new insights into and references for the control and prevention of viral diseases.
Keyphrases
- nuclear factor
- signaling pathway
- lps induced
- pi k akt
- human immunodeficiency virus
- oxidative stress
- sars cov
- toll like receptor
- transcription factor
- inflammatory response
- hepatitis c virus
- randomized controlled trial
- poor prognosis
- gene expression
- hiv positive
- genome wide
- cell proliferation
- drug delivery
- cancer therapy
- hiv aids
- genome wide analysis