Distinct CD55 Isoform Synthesis and Inhibition of Complement-Dependent Cytolysis by Hepatitis C Virus

Kwon, Young‐Chan; Kim, Hangeun; Meyer, Keith; Bisceglie, Adrian M. Di; Ray, Ranjit

doi:10.4049/jimmunol.1600631

Cited by 16 publications

(16 citation statements)

References 59 publications

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“…However, this was reversed when the particles were treated with anti-CD55 and anti-CD59 antibodies or phospholipase C ( 164 ). Although it could well be considered that incorporation is a random process, growing evidences as in the case of HCV, RSV, and PIV5 suggest the recruitment of CD55 and/or CD59 to be more specific in nature because the respective virus infection induced up regulation of the RCAs in infected cells ( 155 , 156 , 165 , 166 ).…”

Section: Complement Evasion By Rna Virusesmentioning

confidence: 99%

In the Crosshairs: RNA Viruses OR Complement?

et al. 2020

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Complement, a part of the innate arm of the immune system, is integral to the frontline defense of the host against innumerable pathogens, which includes RNA viruses. Among the major groups of viruses, RNA viruses contribute significantly to the global mortality and morbidity index associated with viral infection. Despite multiple routes of entry adopted by these viruses, facing complement is inevitable. The initial interaction with complement and the nature of this interaction play an important role in determining host resistance versus susceptibility to the viral infection. Many RNA viruses are potent activators of complement, often resulting in virus neutralization. Yet, another facet of virus-induced activation is the exacerbation in pathogenesis contributing to the overall morbidity. The severity in disease and death associated with RNA virus infections shows a tip in the scale favoring viruses. Growing evidence suggest that like their DNA counterparts, RNA viruses have co-evolved to master ingenious strategies to remarkably restrict complement. Modulation of host genes involved in antiviral responses contributed prominently to the adoption of unique strategies to keep complement at bay, which included either down regulation of activation components (C3, C4) or up regulation of complement regulatory proteins. All this hints at a possible “hijacking” of the cross-talk mechanism of the host immune system. Enveloped RNA viruses have a selective advantage of not only modulating the host responses but also recruiting membrane-associated regulators of complement activation (RCAs). This review aims to highlight the significant progress in the understanding of RNA virus–complement interactions.

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Section: Complement Evasion By Rna Virusesmentioning

confidence: 99%

In the Crosshairs: RNA Viruses OR Complement?

et al. 2020

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“…Since then, CD55 has been characterized as a glycosylphosphatidylinositol-linked membrane protein and has been broadly detected in blood, stroma, epithelial, and endothelial cells ( 14 15 16 ). Additionally, soluble CD55, which was generated by alternative splicing ( 17 ) or matrix metalloproteinase-7 ( 18 ), is distributed in plasma, urine, saliva, tears, and synovial fluids ( 15 ). Glycosylphosphatidylinositol-linked CD55 is regarded as the major form of CD55 rather than soluble CD55 ( 19 ).…”

Section: Cd55mentioning

confidence: 99%

“…Even though the calculated molecular weight of the CD55 protein is 43 kDa, the observed molecular weight of mature CD55 varies between 50 to 100 kDa depending on the cell type ( 8 ). Different sizes of CD55 might be caused by alternative splicing ( 17 20 ) or different glycosylation patterns ( 21 ).…”

Section: Cd55mentioning

confidence: 99%

Beyond the Role of CD55 as a Complement Component

2018

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The complement is a part of the immune system that plays several roles in removing pathogens. Despite the importance of the complement system, the exact role of each component has been overlooked because the complement system was thought to be a nonspecific humoral immune mechanism that worked against pathogens. Decay-accelerating factor (DAF or CD55) is a known inhibitor of the complement system and has recently attracted substantial attention due to its role in various diseases, such as cancer, protein-losing enteropathy, and malaria. Some protein-losing enteropathy cases are caused by CD55 deficiency, which leads to complement hyperactivation, malabsorption, and angiopathic thrombosis. In addition, CD55 has been reported to be an essential host receptor for infection by the malaria parasite. Moreover, CD55 is a ligand of the seven-span transmembrane receptor CD97. Since CD55 is present in various cells, the functional role of CD55 has been expanded by showing that CD55 is associated with a variety of diseases, including cancer, malaria, protein-losing enteropathy, paroxysmal nocturnal hemoglobinuria, and autoimmune diseases. This review summarizes the current understanding of CD55 and the role of CD55 in these diseases. It also provides insight into the development of novel drugs for the diagnosis and treatment of diseases associated with CD55.

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“…HCV induces CD55 as a negative regulator of complement activation and suppresses C3, C4, and C9 complement components of the membrane attack complex. Up‐regulation of CD55 expression on the cell surface or secretion by HCV core protein inhibits complement‐dependent cytolysis . Antibodies against cancer cell‐surface proteins enhance complement‐dependent cytolysis or antibody‐dependent, cell‐mediated cytotoxicity.…”

Section: Innate Immune Response To Hcv Infectionmentioning

confidence: 99%

“…Up-regulation of CD55 expression on the cell surface or secretion by HCV core protein inhibits complement-dependent cytolysis. (39) Antibodies against cancer cell-surface proteins enhance complement-dependent cytolysis or antibody-dependent, cell-mediated cytotoxicity. HCV-induced cell-surface CD55 expression, and secretory CD55 expression in the tumor microenvironment limit complement-mediated damage of HCV-infected cells, favoring cell survival and growth promotion.…”

Section: Complement Regulationmentioning

confidence: 99%

Hepatitis C Virus Manipulates Humans as its Favorite Host for a Long‐Term Relationship

Ray

2019

Hepatology

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Chronic hepatitis C virus (HCV) infection associated liver disease is a global health problem. HCV often causes silent disease, and eventually progresses to end stage liver disease. HCV infects hepatocytes, however initial manifestation of liver disease is mostly displayed in hepatic stellate cells causing fibrosis/cirrhosis, and believed to be occurring from inflammation in the liver. It is still unclear why HCV is not spontaneously cleared from infected liver in the majority of individuals and develops chronic infection with progressive liver disease. Direct-acting antivirals (DAAs) show excellent results in controlling viremia, although beneficial consequence in advanced liver disease remains to be understood. In this review, we highlight the current knowledge that has contributed in our understanding on the role of HCV in inflammation, immune evasion, metabolic disorders, liver pathogeneses, and efforts in vaccine development. This article is protected by copyright. All rights reserved.

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Distinct CD55 Isoform Synthesis and Inhibition of Complement-Dependent Cytolysis by Hepatitis C Virus

Cited by 16 publications

References 59 publications

In the Crosshairs: RNA Viruses OR Complement?

In the Crosshairs: RNA Viruses OR Complement?

Beyond the Role of CD55 as a Complement Component

Hepatitis C Virus Manipulates Humans as its Favorite Host for a Long‐Term Relationship

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