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Antiviral Protection via RdRP-Mediat...

Painter, Meghan M.

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Antiviral Protection via RdRP-Mediatedy Stable Activation of Innate Immunit.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Antiviral Protection via RdRP-Mediatedy Stable Activation of Innate Immunit./
Author:	Painter, Meghan M.
Description:	171 p.
Notes:	Source: Dissertation Abstracts International, Volume: 77-10(E), Section: B.
Contained By:	Dissertation Abstracts International77-10B(E).
Subject:	Virology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10111500
ISBN:	9781339747095

Antiviral Protection via RdRP-Mediatedy Stable Activation of Innate Immunit.
Painter, Meghan M.

Antiviral Protection via RdRP-Mediatedy Stable Activation of Innate Immunit. - 171 p.

Source: Dissertation Abstracts International, Volume: 77-10(E), Section: B.

Thesis (Ph.D.)--College of Medicine - Mayo Clinic, 2015.

All RNA viruses encode RNA-dependent RNA polymerases (RdRPs) which produce viral replication intermediates that trigger acute innate immune activation through sensors such as TLR3, RIG-I and MDA5. Mammalian genomes lack RdRPs, and RNA viruses sequester them tightly within specialized membranous compartments. This concentrates the viral synthetic apparatus and may also function in immune sensor avoidance. Our data show that the ectopic expression of a viral RdRP profoundly reconfigures innate immunity; requiring RdRP-catalysis which produces double-stranded RNA, it confers MDA5-MAVS-mediated constitutive innate immune system activation.

ISBN: 9781339747095Subjects--Topical Terms:

642304
Virology.

Antiviral Protection via RdRP-Mediatedy Stable Activation of Innate Immunit.
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245 1 0 $a Antiviral Protection via RdRP-Mediatedy Stable Activation of Innate Immunit.
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500 $a Source: Dissertation Abstracts International, Volume: 77-10(E), Section: B.
500 $a Adviser: Moses Rodriguez.
502 $a Thesis (Ph.D.)--College of Medicine - Mayo Clinic, 2015.
520 $a All RNA viruses encode RNA-dependent RNA polymerases (RdRPs) which produce viral replication intermediates that trigger acute innate immune activation through sensors such as TLR3, RIG-I and MDA5. Mammalian genomes lack RdRPs, and RNA viruses sequester them tightly within specialized membranous compartments. This concentrates the viral synthetic apparatus and may also function in immune sensor avoidance. Our data show that the ectopic expression of a viral RdRP profoundly reconfigures innate immunity; requiring RdRP-catalysis which produces double-stranded RNA, it confers MDA5-MAVS-mediated constitutive innate immune system activation.
520 $a Our experiments demonstrated that uninfected RdRP-transgenic mice display life-long, quantitatively-dramatic upregulation (up to 300-fold) of a potent panel of interferon-stimulated genes (ISGs). These mice exhibit profound resistance to normally lethal viral challenges via a mechanism that is independent of (Rag1) adaptive immunity. Importantly, despite their lifelong ISG elevations, RdRP mice do not have chronic inflammatory pathologies and are entirely healthy, with normal longevity. The system could be recapitulated in human cells with striking fidelity to the mouse: the RdRP induced an analogous stable ISG network that restricted HIV-1 infection. Our data reveal that a powerfully augmented MDA5-dependent activation state can be a well-tolerated innate immune system configuration. In addition to this key insight, we show that an elevated basal ISG profile provides in vivo and in vitro protection from viral infection. This research supplies a foundation for augmenting innate immunity to achieve broad-spectrum antiviral protection.
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