J Virol 89:10489–10499Īrndt WD, White SD, Johnson BP, Huynh T, Liao J, Harrington H, Cotsmire S, Kibler KV, Langland J, Jacobs BL (2016) Monkeypox virus induces the synthesis of less dsRNA than vaccinia virus, and is more resistant to the anti-poxvirus drug, IBT, than vaccinia virus. Immunol Cell Biol 86:239–245Īrndt WD, Cotsmire S, Trainor K, Harrington H, Hauns K, Kibler KV, Huynh TP, Jacobs BL (2015) Evasion of the innate immune type I interferon system by Monkeypox virus. Virology 202:305–314Īlsharifi M, Mullbacher A, Regner M (2008) Interferon type I responses in primary and secondary infections. Single-stranded ribose nucleic acid TMBIM:Īli AN, Turner PC, Brooks MA, Moyer RW (1994) The SPI-1 gene of rabbitpox virus determines host range and is required for hemorrhagic pock formation. Receptor interacting protein kinase RNase: Pathogen-associated molecular patterns PRRs: Nucleotide-binding oligomerization domain PAMPs: KeywordsĪpoptosis-associated speck like proteins BH3:Ĭaspase activation and recruitment domain DAMPs:ĭouble-stranded RNA-dependent protein kinase eIF2α: 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. Recently described viral mimics of MLKL in other chordopoxviruses inhibit all three modes of necroptotic cell death. 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. 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. 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). More recently, they have been shown to inhibit necroptotic cell death through two distinct strategies. Poxviruses have been long regarded as potent inhibitors of apoptotic cell death.
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