scholarly journals Viral Induced Protein Aggregation: A Mechanism of Immune Evasion

2021 ◽  
Vol 22 (17) ◽  
pp. 9624
Author(s):  
Elena Muscolino ◽  
Laura-Marie Luoto ◽  
Wolfram Brune
Keyword(s):  
Protein Aggregation ◽  
Immune Evasion ◽  
Defense Mechanism ◽  
Cellular Protein ◽  
Aggregate Formation ◽  
Extrinsic Factors ◽  
Cytotoxic Effects ◽  
Cellular Defense ◽  
Viral Immune Evasion ◽  
Ribonucleotide Reductases

Various intrinsic and extrinsic factors can interfere with the process of protein folding, resulting in protein aggregates. Usually, cells prevent the formation of aggregates or degrade them to prevent the cytotoxic effects they may cause. However, during viral infection, the formation of aggregates may serve as a cellular defense mechanism. On the other hand, some viruses are able to exploit the process of aggregate formation and removal to promote their replication or evade the immune response. This review article summarizes the process of cellular protein aggregation and gives examples of how different viruses exploit it. Particular emphasis is placed on the ribonucleotide reductases of herpesviruses and how their additional non-canonical functions in viral immune evasion are closely linked to protein aggregation.

Role of Histamine and Leucotaxin in Function of Cellular Defense Mechanism

1956 ◽  
Vol 184 (2) ◽  
pp. 296-300 ◽  
Author(s):  
László Kátó ◽  
Béla Gözsy
Keyword(s):  
Fluid Flow ◽  
Tissue Damage ◽  
Inflammatory Process ◽  
Defense Mechanism ◽  
Volatile Oils ◽  
Time Intervals ◽  
Cellular Defense ◽  
Intradermal Administration ◽  
Flow Through

Experiments are presented to the effect that in an inflammatory process histamine and leucotaxin appear successively at different and orderly time intervals, thus assuring an increased fluid flow through the capillary wall. Histamine is released not only in the inflammatory process but also by intradermal administration of such substances (volatile oils or their components) which induce neither the triple response of Th. Lewis nor any tissue damage. This could be explained by the fact that in the tissues histamine is ‘present’ but leucotaxin is ‘formed.’

scholarly journals Activation of Cellular Defense Mechanism by Organic-Inorganic Hybrid Molecules

2014 ◽  
Vol 134 (7) ◽  
pp. 813-815
Author(s):  
Tomoya Fujie ◽  
Hiroshi Naka ◽  
Chika Yamamoto ◽  
Yasuhiro Shinkai ◽  
Yoshito Kumagai ◽  
...  
Keyword(s):  
Defense Mechanism ◽  
Inorganic Hybrid ◽  
Cellular Defense ◽  
Hybrid Molecules

scholarly journals Antioxidative defense

2011 ◽  
Vol 65 (3-4) ◽  
pp. 247-256
Author(s):  
Jelka Stevanovic ◽  
Suncica Borozan ◽  
Slavoljub Jovic ◽  
Igor Ignjatovic
Keyword(s):  
Free Radicals ◽  
Glutathione Peroxidase ◽  
Coenzyme Q ◽  
Cellular Protein ◽  
The Body ◽  
Antioxidative Defense ◽  
Cellular Defense ◽  
Physiological Processes ◽  
Vitamins E And C ◽  
And Control

Free radicals occur constantly during metabolism and take part in numerous physiological processes, such as: intra-cellular and inter-cellular signalization, gene expression, removal of damaged or senescent cells, and control of the tone of blood vessels. However, there is an increased quantity of free radicals in situations of so-called oxidative stress, when they cause serious damage to cellular membranes (peroxidation of their lipids, damage of membrane proteins, and similar), to interior cellular protein molecules, as well as DNA molecules and carbohydrates. This is precisely why the organism has developed numerous mechanisms for removing free radicals and/or preventing their production. Some of these are enzyme-related and include superoxide-dismutase, catalase, glutathione-peroxidase, and others. Other, non-enzyme mechanisms, imply antioxidative activities of vitamins E and C, provitamin A, coenzyme Q, reduced glutation, and others. Since free radicals can leave the cell that has produced them and become dispersed throughout the body, in addition to antioxidative defense that functions within cellular structures, antioxidant extra-cellular defense has also been developed. This is comprised by: transferrin, lactoferrin, haptoglobin, hemopexin, ceruloplasmin, albumins, extra-cellular isoform SOD, extracellular glutathione-peroxidase, glucose, bilirubin, urates, and many other molecules.

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.

New insights into the structure of the MHC class I peptide-loading complex and mechanisms of TAP inhibition by viral immune evasion proteins

2019 ◽  
Vol 113 ◽  
pp. 103-114 ◽  
Author(s):  
Patrique Praest ◽  
A. Manuel Liaci ◽  
Friedrich Förster ◽  
Emmanuel J.H.J. Wiertz
Keyword(s):  
Mhc Class I ◽  
Immune Evasion ◽  
Class I ◽  
Viral Immune Evasion ◽  
Peptide Loading

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.

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