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Gem

Defective Viral Genomes: Critical Danger Signals of Viral Infections

Carolina B. López
S. Schultz-Cherry, Editor
Carolina B. López
Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
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S. Schultz-Cherry
Roles: Editor
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DOI: 10.1128/JVI.00707-14
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    Current and proposed models of the events required for the development of effective antiviral responses to infections with paramyxoviruses. (A) According to current paradigms, viral recognition is maximized by type I IFN signaling that promotes the expression of essential viral sensors and signaling molecules. This paradigm assumes a low level of expression of type I IFN. In the depicted example of SeV infection, this scenario is possible if the virus-encoded V and C antagonistic proteins are only partially active, for example, during a zoonotic infection. However, this scenario cannot explain the induction of the antiviral response in the natural host of this virus, which is effectively blocked by the viral antagonists. (B) The model developed by my laboratory proposes that defective viral genomes that arise at high levels of virus replication provide potent danger signals that stimulate the host antiviral response to overcome viral antagonism, independently of type I IFN feedback.

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Defective Viral Genomes: Critical Danger Signals of Viral Infections
Carolina B. López
Journal of Virology Jul 2014, 88 (16) 8720-8723; DOI: 10.1128/JVI.00707-14

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Defective Viral Genomes: Critical Danger Signals of Viral Infections
Carolina B. López
Journal of Virology Jul 2014, 88 (16) 8720-8723; DOI: 10.1128/JVI.00707-14
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    • ABSTRACT
    • BATTLE FOR VIRUS AND HOST COEXISTENCE
    • ORIGIN AND ACTIVITY OF DVGs
    • CELLULAR RESPONSE TO DVGs
    • IMMUNOSTIMULATORY MOLECULAR MOTIFS OF DVGs
    • DVGs IN NATURAL INFECTIONS
    • CONTRIBUTIONS TO THE FIELD AND FUTURE DIRECTIONS
    • ACKNOWLEDGMENTS
    • FOOTNOTES
    • REFERENCES
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