Abstract

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.

Highlights

  • The nuclear factor-κB (NF-κB) family is composed of five related transcription factors: p50, p52, p65, c-Rel, and RelB

  • MyD88 activates interleukin-1 receptor-associated kinases (IRAKs) and TNFR-associated associated factor 6 (TRAF6), mitochondrial antiviral signaling protein (MAVS) interacts with TRAF6, and TRIF interacts with receptor interacting protein 1 (RIP1)

  • Hepatitis E virus (HEV) open reading frame 3 (ORF3) encodes a protein that blocks the Nuclear factor-κB (NF-κB) signaling pathway through reducing the levels of transcription and translation of TLR4, TRAF6, and nucleotide-binding oligomerization domain containing 2 (NOD2), a receptor associated with the bacterial adaptor molecule [22]

Read more

Summary

Introduction

The nuclear factor-κB (NF-κB) family is composed of five related transcription factors: p50, p52, p65, c-Rel, and RelB. Course of against evolution, viruses have NF-κB developed major role in innate immune responses by inducing antiviral genes, such as interferon (IFN) and IFNmethods that interfere with NF-κB activity to promote viral survival. To better understand the role of NF-κB proteases, viral deubiquitinating enzymes (DUBs), phosphodegron-like (PDL) motifs, viral protein in viral phosphatase immune escape, we use human immunodeficiency virus 1 (HIV-1) as an example, and describe (PPase)-binding proteins, and small hydrophobic (SH) proteins. HIV-1weimmune escape in different viral cycles:asproductive the role of NF-κBactivity in viral promotes immune escape, use human immunodeficiency viruslife. Weinhibiting hope that this activity review promotes can provide a reference for the and and infection.

The Activation of the NF-κB
Receptors
Adaptor Proteins
Targeting Receptors and Adaptor Proteins
Targeting IKKs
Targeting IκBα
Proteases Encoded by Viruses
The 3C and 3C-Like Proteases
DUBs Encoded by Viruses
Other Viral DUBs
PDL Motifs Encoded by Viruses
PPase-Binding Proteins Encoded by Viruses
SH Protein Encoded by Viruses
Suppression of NF-κB Activity to Facilitate HIV-1 Immune Evasion
Conclusions
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call