Current Topics in Microbiology and Immunology Ser.: Alternate Programmed Cell Death Signaling in Antiviral Host Defense by Pratyusha Mandal (2023, Hardcover)

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This transformative evidence identified a novel pathway acting independent of TNF, interferon or RIPK1 that can stop virus from infecting its natural mouse host by killing off infected cells to halt replication.

About this product

Product Identifiers

Publisher
Springer International Publishing A&G
ISBN-10
3031452771
ISBN-13
9783031452772
eBay Product ID (ePID)
15062642092

Product Key Features

Number of Pages
V, 174 Pages
Publication Name
Alternate Programmed Cell Death Signaling in Antiviral Host Defense
Language
English
Publication Year
2023
Subject
Life Sciences / Microbiology, Life Sciences / Virology, Immunology, Microbiology
Type
Textbook
Author
Pratyusha Mandal
Subject Area
Science, Medical
Series
Current Topics in Microbiology and Immunology Ser.
Format
Hardcover

Dimensions

Item Weight
15.6 Oz
Item Length
9.3 in
Item Width
6.1 in

Additional Product Features

Dewey Edition
23
Series Volume Number
442
Number of Volumes
1 vol.
Illustrated
Yes
Dewey Decimal
616.9101
Table Of Content
Programmed Necrosis in Host Defense.- ZBP1/DAI-dependent Cell Death Pathways in Influenza A Virus Immunity and Pathogenesis.- Pyroptosis in Antiviral Immunity.- Manipulation of Host Cell Death Pathways by Herpes Simplex Virus.- Subversion of Programed Cell Death by Poxviruses.- Cell Killing by Reovirus: Mechanisms and Consequences.- Outcomes of RIP kinase signaling during neuroinvasive viral infection.
Synopsis
This volume provides a comprehensive review of programmed cell death pathways and their fundamental role in antiviral host defense. The book deep-dives into the molecular functions and regulation of necroptosis and discusses how viruses induce and manipulate this potent innate cellular sensing system. Initially, understanding of necroptosis emerged from studies on tumor necrosis factor (TNF) signaling that showed the key role of receptor interacting protein kinase 1 (RIPK1) in the activation of receptor interacting protein kinase 3 (RIPK3) which then phosphorylates mixed lineage kinase domain like pseudokinase (MLKL) to execute cells via plasma membrane leakage of cytosolic contents. Since its discovery, multiple facets of the RIPK3-dependent necroptotic machinery have evolved where the requirements for execution of death varies depending on the stimulus. Virus-induced necroptosis was discovered over 10 years ago in studies on murine cytomegalovirus (MCMV)where a virus-encoded inhibitor was shown to prevent the recruitment of RIPK3 (RIP3). This transformative evidence identified a novel pathway acting independent of TNF, interferon or RIPK1 that can stop virus from infecting its natural mouse host by killing off infected cells to halt replication. Over the past decade influenza A virus (IAV), herpes simplex virus (HSV) and poxvirus vaccinia (VACV) have all been shown to trigger the pathway. Herpesviruses and poxviruses also encode inhibitors of caspase-8 whose elaboration unleashes the necroptosis pathway. IAV and other RNA viruses do not encode programmed cell death inhibitors. RIPK3 is also known to induce apoptosis by recruiting RIPK1 as shown nearly a decade ago and this dual apoptosis/necroptosis induction occurs naturally during influenza A virus infection. RIPK3 is also able to induce an inflammatory response independently of programmed cell death that can predominate to drive inflammatory disease outcomes. This volume is a must-read for researchers and advanced students in immunology and virology.
LC Classification Number
QR180-189.5

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Current Topics in Microbiology and Immunology Ser.: Alternate Programmed Cell Death Signaling in Antiviral Host Defense by Pratyusha Mandal (2023, Hardcover)

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All listings for this product

item 1 Alternate Programmed Cell Death Signaling in Antiviral Host Defense, Hardcove...

item 2 Alternate Programmed Cell Death Signaling in Antiviral Host Defense, Hardcove...

item 3 Alternate Programmed Cell Death Signaling in Antiviral Host Defense by Edward S.

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