Viral-derived complement inhibitors: current status and potential role in immunomodulation
Loading...
Date
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
SAGE Publications Inc.
Abstract
The complement system is one of the body’s major innate immune defense mechanisms in vertebrates. Its function is to detect foreign bodies and promote their elimination through opsonisation or lysis. Complement proteins play an important role in the immunopathogenesis of several disorders. However, excessive complement activation does not confer more protection but instead leads to several autoimmune and inflammatory diseases. With inappropriate activation of the complement system, activated complement proteins and glycoproteins may damage both healthy and diseased tissues. Development of complement inhibitors represents an effective approach in controlling dysregulated complement activity and reducing disease severity, yet few studies have investigated the nature and role of novel complement inhibitory proteins of viral origin. Viral complement inhibitors have important implications in understanding the importance of complement inhibition and their role as a promising novel therapeutic approach in diseases caused by dysregulated complement function. In this review, we discuss the role and importance of complement inhibitors derived from several viruses in the scope of human inflammatory and autoimmune diseases. © 2016, © 2016 by the Society for Experimental Biology and Medicine.
Description
Keywords
Complement, Complement inhibitor, Complement regulation, Disease, Inflammation, Virus, Animals, Autoimmune diseases, Complement activation, Complement inactivating agents, Complement system proteins, Humans, Immunomodulation, Mice, Viral proteins, Virus diseases, Viruses, Antivirus agent, Coat protein, Hepatitis b virus x protein, Nonstructural protein 1, Viral protein, Article, Astrovirus infection, Atherosclerosis, Autoimmune disease, Blood transfusion, Complement system, Disease severity, Flaviviridae, Hepatitis b virus, Herpes simplex virus 1, Human, Inflammatory disease, Innate immunity, Macular degeneration, Membranoproliferative glomerulonephritis, Neutrophil chemotaxis, Nipah virus, Nonhuman, Opsonization, Phagocytosis, Poxviridae, Reperfusion injury, West nile virus, Animal, Immunology, Metabolism, Mouse, Virus infection