Abstract:
:Poxviruses have been long regarded as potent inhibitors of apoptotic cell death. More recently, they have been shown to inhibit necroptotic cell death through two distinct strategies. These strategies involve either blocking virus sensing by the host pattern recognition receptor, ZBP1 (also called DAI) or by influencing receptor interacting protein kinase (RIPK)3 signal transduction by inhibition of activation of the executioner of necroptosis, mixed lineage kinase-like protein (MLKL). Vaccinia virus E3 specifically blocks ZBP1 → RIPK3 → MLKL necroptosis, leaving virus-infected cells susceptible to the TNF death-receptor signaling (e.g., TNFR1 → FADD → RIPK1 → RIPK3 → MLKL), and, potentially, TLR3 → TRIF → RIPK3 → MLKL necroptosis. While E3 restriction of necroptosis appears to be common to many poxviruses that infect vertebrate hosts, another modulatory strategy not observed in vaccinia or variola virus manifests through subversion of MLKL activation. Recently described viral mimics of MLKL in other chordopoxviruses inhibit all three modes of necroptotic cell death. As with inhibition of apoptosis, the evolution of potentially redundant viral mechanisms to inhibit programmed necroptotic cell death emphasizes the importance of this pathway in the arms race between pathogens and their hosts.
journal_name
Curr Top Microbiol Immunoljournal_title
Current topics in microbiology and immunologyauthors
Koehler HS,Jacobs BLdoi
10.1007/82_2020_229subject
Has Abstractpub_date
2021-01-29 00:00:00eissn
0070-217Xissn
2196-9965pub_type
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