Abstract
The interferon system protects mammals against virus infections. There are several types of interferons, which are characterized by their ability to inhibit virus replication and resultant pathogenesis by triggering both innate and cell-mediated immune responses. Virus infection is sensed by a variety of cellular pattern-recognition receptors and triggers the synthesis of interferons, which are secreted by the infected cells. In uninfected cells, cell surface receptors recognize the secreted interferons and activate intracellular signaling pathways that induce the expression of interferon-stimulated genes; the proteins encoded by these genes inhibit different stages of virus replication. To avoid extinction, almost all viruses have evolved mechanisms to defend themselves against the interferon system. Consequently, a dynamic equilibrium of survival is established between the virus and its host, an equilibrium that can be shifted to the host's favor by the use of exogenous interferon as a therapeutic antiviral agent.
Original language | English |
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Pages (from-to) | 549-572 |
Number of pages | 24 |
Journal | Annual Review of Virology |
Volume | 2 |
DOIs | |
State | Published - Nov 9 2015 |
Bibliographical note
Publisher Copyright:Copyright © 2015 by Annual Reviews. All rights reserved.
Funding
Funders | Funder number |
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National Institutes of Health (NIH) | CA068782, AI073303, CA062220 |
National Childhood Cancer Registry – National Cancer Institute | R01CA068782 |
Keywords
- Antiviral action
- DsRNA
- Innate immunity
- Interferon-stimulated gene
- Interferon-λ
- Pathogenesis
- Pattern-recognition receptor
- Viral evasion
- Virus infection
ASJC Scopus subject areas
- Virology