Picornaviruses and Apoptosis: Subversion of Cell Death

Sarah CROFT, Erin WALKER, Reena GHILDYAL

    Research output: Contribution to journalArticle

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    Abstract

    Infected cells can undergo apoptosis as a protective response to viral infection, thereby limiting viral infection. As viruses require a viable cell for replication, the death of the cell limits cellular functions that are required for virus replication and propagation. Picornaviruses are single-stranded RNA viruses that modify the host cell apoptotic response, probably in order to promote viral replication, largely as a function of the viral proteases 2A, 3C, and 3CD. These proteases are essential for viral polyprotein processing and also cleave cellular proteins. Picornavirus proteases cleave proapoptotic adaptor proteins, resulting in downregulation of apoptosis. Picornavirus proteases also cleave nucleoporins, disrupting the orchestrated manner in which signaling pathways use active nucleocytoplasmic trafficking, including those involved in apoptosis. In addition to viral proteases, the transmembrane 2B protein alters intracellular ion signaling, which may also modulate apoptosis. Overall, picornaviruses, via the action of virally encoded proteins, exercise intricate control over and subvert cell death pathways, specifically apoptosis, thereby allowing viral replication to continue.
    Original languageEnglish
    Article numbere01009-17
    Pages (from-to)1-13
    Number of pages13
    JournalmBio
    Volume8
    Issue number5
    DOIs
    Publication statusPublished - 2017

    Fingerprint

    Picornaviridae
    Cell Death
    Apoptosis
    Peptide Hydrolases
    Virus Diseases
    Proteins
    Nuclear Pore Complex Proteins
    Polyproteins
    RNA Viruses
    Virus Replication
    Down-Regulation
    Ions
    Viruses

    Cite this

    CROFT, Sarah ; WALKER, Erin ; GHILDYAL, Reena. / Picornaviruses and Apoptosis: Subversion of Cell Death. In: mBio. 2017 ; Vol. 8, No. 5. pp. 1-13.
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    title = "Picornaviruses and Apoptosis: Subversion of Cell Death",
    abstract = "Infected cells can undergo apoptosis as a protective response to viral infection, thereby limiting viral infection. As viruses require a viable cell for replication, the death of the cell limits cellular functions that are required for virus replication and propagation. Picornaviruses are single-stranded RNA viruses that modify the host cell apoptotic response, probably in order to promote viral replication, largely as a function of the viral proteases 2A, 3C, and 3CD. These proteases are essential for viral polyprotein processing and also cleave cellular proteins. Picornavirus proteases cleave proapoptotic adaptor proteins, resulting in downregulation of apoptosis. Picornavirus proteases also cleave nucleoporins, disrupting the orchestrated manner in which signaling pathways use active nucleocytoplasmic trafficking, including those involved in apoptosis. In addition to viral proteases, the transmembrane 2B protein alters intracellular ion signaling, which may also modulate apoptosis. Overall, picornaviruses, via the action of virally encoded proteins, exercise intricate control over and subvert cell death pathways, specifically apoptosis, thereby allowing viral replication to continue.",
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    Picornaviruses and Apoptosis: Subversion of Cell Death. / CROFT, Sarah; WALKER, Erin; GHILDYAL, Reena.

    In: mBio, Vol. 8, No. 5, e01009-17, 2017, p. 1-13.

    Research output: Contribution to journalArticle

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    T1 - Picornaviruses and Apoptosis: Subversion of Cell Death

    AU - CROFT, Sarah

    AU - WALKER, Erin

    AU - GHILDYAL, Reena

    PY - 2017

    Y1 - 2017

    N2 - Infected cells can undergo apoptosis as a protective response to viral infection, thereby limiting viral infection. As viruses require a viable cell for replication, the death of the cell limits cellular functions that are required for virus replication and propagation. Picornaviruses are single-stranded RNA viruses that modify the host cell apoptotic response, probably in order to promote viral replication, largely as a function of the viral proteases 2A, 3C, and 3CD. These proteases are essential for viral polyprotein processing and also cleave cellular proteins. Picornavirus proteases cleave proapoptotic adaptor proteins, resulting in downregulation of apoptosis. Picornavirus proteases also cleave nucleoporins, disrupting the orchestrated manner in which signaling pathways use active nucleocytoplasmic trafficking, including those involved in apoptosis. In addition to viral proteases, the transmembrane 2B protein alters intracellular ion signaling, which may also modulate apoptosis. Overall, picornaviruses, via the action of virally encoded proteins, exercise intricate control over and subvert cell death pathways, specifically apoptosis, thereby allowing viral replication to continue.

    AB - Infected cells can undergo apoptosis as a protective response to viral infection, thereby limiting viral infection. As viruses require a viable cell for replication, the death of the cell limits cellular functions that are required for virus replication and propagation. Picornaviruses are single-stranded RNA viruses that modify the host cell apoptotic response, probably in order to promote viral replication, largely as a function of the viral proteases 2A, 3C, and 3CD. These proteases are essential for viral polyprotein processing and also cleave cellular proteins. Picornavirus proteases cleave proapoptotic adaptor proteins, resulting in downregulation of apoptosis. Picornavirus proteases also cleave nucleoporins, disrupting the orchestrated manner in which signaling pathways use active nucleocytoplasmic trafficking, including those involved in apoptosis. In addition to viral proteases, the transmembrane 2B protein alters intracellular ion signaling, which may also modulate apoptosis. Overall, picornaviruses, via the action of virally encoded proteins, exercise intricate control over and subvert cell death pathways, specifically apoptosis, thereby allowing viral replication to continue.

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    KW - Host-Pathogen Interactions

    KW - Immunity

    KW - Virus Replication

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