scholarly journals Suppression of NF-κB Activity: A Viral Immune Evasion Mechanism

Viruses ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 409 ◽  
Author(s):  
Liyao Deng ◽  
Qiurui Zeng ◽  
Mingshu Wang ◽  
Anchun Cheng ◽  
Renyong Jia ◽  
...  
Keyword(s):  
Immune Evasion ◽  
Adaptor Proteins ◽  
Nuclear Factor Κb ◽  
Deubiquitinating Enzymes ◽  
Immune Evasion Mechanism ◽  
Viral Immune Evasion ◽  
Antiviral Genes ◽  
Immunodeficiency Virus ◽  
Control And Prevention ◽  
Small Hydrophobic

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.

scholarly journals Hantavirus-Driven PD-L1/PD-L2 Upregulation: An Imperfect Viral Immune Evasion Mechanism

2018 ◽  
Vol 9 ◽  
Author(s):  
Martin J. Raftery ◽  
Mohammed O. Abdelaziz ◽  
Jörg Hofmann ◽  
Günther Schönrich
Keyword(s):  
Immune Evasion ◽  
Immune Evasion Mechanism ◽  
Viral Immune Evasion

scholarly journals The complex of MCMV proteins and MHC class I evades NK cell control and drives the evolution of virus-specific activating Ly49 receptors

2019 ◽  
Vol 216 (8) ◽  
pp. 1809-1827 ◽  
Author(s):  
Jelena Železnjak ◽  
Vanda Juranić Lisnić ◽  
Branka Popović ◽  
Berislav Lisnić ◽  
Marina Babić ◽  
...  
Keyword(s):  
Nk Cells ◽  
Immune Evasion ◽  
Nk Cell ◽  
Cytotoxic T Cells ◽  
Mhc I ◽  
Immune Evasion Mechanism ◽  
Viral Immune Evasion ◽  
Nk Cell Receptors ◽  
Self Recognition ◽  
Missing Self

CMVs efficiently target MHC I molecules to avoid recognition by cytotoxic T cells. However, the lack of MHC I on the cell surface renders the infected cell susceptible to NK cell killing upon missing self recognition. To counter this, mouse CMV (MCMV) rescues some MHC I molecules to engage inhibitory Ly49 receptors. Here we identify a new viral protein, MATp1, that is essential for MHC I surface rescue. Rescued altered-self MHC I molecules show increased affinity to inhibitory Ly49 receptors, resulting in inhibition of NK cells despite substantially reduced MHC I surface levels. This enables the virus to evade recognition by licensed NK cells. During evolution, this novel viral immune evasion mechanism could have prompted the development of activating NK cell receptors that are specific for MATp1-modified altered-self MHC I molecules. Our study solves a long-standing conundrum of how MCMV avoids recognition by NK cells, unravels a fundamental new viral immune evasion mechanism, and demonstrates how this forced the evolution of virus-specific activating MHC I–restricted Ly49 receptors.

scholarly journals Pathogenic Role of Immune Evasion and Integration of Human Papillomavirus in Oropharyngeal Cancer

2021 ◽  
Vol 9 (5) ◽  
pp. 891
Author(s):  
Takashi Hatano ◽  
Daisuke Sano ◽  
Hideaki Takahashi ◽  
Nobuhiko Oridate
Keyword(s):  
Human Papillomavirus ◽  
Immune Evasion ◽  
Oropharyngeal Cancer ◽  
Current Knowledge ◽  
Immune Evasion Mechanism ◽  
Cell Cycle Activation ◽  
Genome Integration ◽  
Integration Mechanisms ◽  
E6 And E7

The incidence of oropharyngeal cancer (OPC) is increasing remarkably among all head and neck cancers, mainly due to its association with the human papillomavirus (HPV). Most HPVs are eliminated by the host’s immune system; however, because HPV has developed an effective immune evasion mechanism to complete its replication cycle, a small number of HPVs are not eliminated, leading to persistent infection. Moreover, during the oncogenic process, the extrachromosomal HPV genome often becomes integrated into the host genome. Integration involves the induction and high expression of E6 and E7, leading to cell cycle activation and increased genomic instability in the host. Therefore, integration is an important event in oncogenesis, although the associated mechanism remains unclear, especially in HPV-OPC. In this review, we summarize the current knowledge on HPV-mediated carcinogenesis, with special emphasis on immune evasion and integration mechanisms, which are crucial for oncogenesis.

scholarly journals Structure, Function, and Interactions of the HIV-1 Capsid Protein

Life ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 100
Author(s):  
Eric Rossi ◽  
Megan E. Meuser ◽  
Camille J. Cunanan ◽  
Simon Cocklin
Keyword(s):  
Life Cycle ◽  
Capsid Protein ◽  
Adaptor Proteins ◽  
Restriction Factors ◽  
Gag Polyprotein ◽  
Immunodeficiency Virus ◽  
Host Cell Factors ◽  
Hiv 1

The capsid (CA) protein of the human immunodeficiency virus type 1 (HIV-1) is an essential structural component of a virion and facilitates many crucial life cycle steps through interactions with host cell factors. Capsid shields the reverse transcription complex from restriction factors while it enables trafficking to the nucleus by hijacking various adaptor proteins, such as FEZ1 and BICD2. In addition, the capsid facilitates the import and localization of the viral complex in the nucleus through interaction with NUP153, NUP358, TNPO3, and CPSF-6. In the later stages of the HIV-1 life cycle, CA plays an essential role in the maturation step as a constituent of the Gag polyprotein. In the final phase of maturation, Gag is cleaved, and CA is released, allowing for the assembly of CA into a fullerene cone, known as the capsid core. The fullerene cone consists of ~250 CA hexamers and 12 CA pentamers and encloses the viral genome and other essential viral proteins for the next round of infection. As research continues to elucidate the role of CA in the HIV-1 life cycle and the importance of the capsid protein becomes more apparent, CA displays potential as a therapeutic target for the development of HIV-1 inhibitors.

scholarly journals Structure of the Infective Getah Virus at 2.8 Å-resolution Determined by Cryo-electron Microscopy

2021 ◽  
Author(s):  
Aojie Wang ◽  
Feng Zhou ◽  
Congcong Liu ◽  
Dongsheng Gao ◽  
Ruxi Qi ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Immune Evasion ◽  
Cell Invasion ◽  
Structural Information ◽  
Host Cell Invasion ◽  
Hydrophobic Pocket ◽  
Viral Immune Evasion ◽  
Cryo Electron Microscopy ◽  
Reproductive Losses ◽  
Getah Virus

Getah virus (GETV) is a mosquito-borne pathogen that can cause a mild illness and reproductive losses in animals. Although antibodies to GETV have been found in humans, there are no reports of clinical symptom associated with GETV. However, antivirals or vaccine against GETV is still unavailable due to lack of knowledge of the structure of GETV virion. Here, we present the structure of mature GETV at a resolution of 2.8 Å with capsid protein, envelope glycoproteins E1 and E2. Glycosylation and S-acylation sites in E1 and E2 are identified. The surface-exposed glycans demonstrated their impact on the viral immune evasion and host cell invasion. The S-acylation sites strongly stabilize the virion. In addition, a cholesterol and phospholipid molecule are observed in transmembrane hydrophobic pocket, together with two more cholesterols surround the pocket. These structural information are helpful for structure-based antivirals and vaccine design.

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