Invasion of host cell by a virus leads to changes in multiple signaling pathways. As a first line of defense innate immune signaling pathways are activated by the host cell to act against the invading virus. Recognition of viral nucleic acid or gene products leads to activation of signaling cascades resulting in expression of variety of anti-viral proteins. These signal-transduction pathways are tightly regulated by post-translational modifications by covalent attachment of ubiquitin (Ub) and ubiquitin-like (UbL) polypeptides, such as ISG15, SUMO, NEDD8 etc. In order to evade the host-innate immune responses viruses have also developed strategies that target the components of Ub and UbL modifications. They do so by hijacking the cellular components of the Ub and UbL conjugation machineries that can redirect the host conjugation machinery to number of cellular substrates for proteasomal degradation or they encode functional homologs of deconjugases and ligases to interfere with UbL-dependent processes. In this Research Topic we aim to enhance our current understanding of the inter-play between viruses and Ub and UbL pathways.
The Research Topic will accept Review articles, Mini-reviews, Original research articles and Perspectives that will give updated insight that cover, but are not limited to, the following topics:
i) Ub and UbL signaling in regulation of innate immune responses during viral infection
ii) Regulation of innate immune defenses by Ubiquitin-like modifiers such as ISG15, SUMO, Nedd8 etc.
iii) Role of Viral deconjugases in immune evasion
iv) Virus mediated Ub and UbL modifications
v) Methods to study Ub and UbL modifications during virus infection
vi) Novel antiviral targets in the ubiquitin system
Invasion of host cell by a virus leads to changes in multiple signaling pathways. As a first line of defense innate immune signaling pathways are activated by the host cell to act against the invading virus. Recognition of viral nucleic acid or gene products leads to activation of signaling cascades resulting in expression of variety of anti-viral proteins. These signal-transduction pathways are tightly regulated by post-translational modifications by covalent attachment of ubiquitin (Ub) and ubiquitin-like (UbL) polypeptides, such as ISG15, SUMO, NEDD8 etc. In order to evade the host-innate immune responses viruses have also developed strategies that target the components of Ub and UbL modifications. They do so by hijacking the cellular components of the Ub and UbL conjugation machineries that can redirect the host conjugation machinery to number of cellular substrates for proteasomal degradation or they encode functional homologs of deconjugases and ligases to interfere with UbL-dependent processes. In this Research Topic we aim to enhance our current understanding of the inter-play between viruses and Ub and UbL pathways.
The Research Topic will accept Review articles, Mini-reviews, Original research articles and Perspectives that will give updated insight that cover, but are not limited to, the following topics:
i) Ub and UbL signaling in regulation of innate immune responses during viral infection
ii) Regulation of innate immune defenses by Ubiquitin-like modifiers such as ISG15, SUMO, Nedd8 etc.
iii) Role of Viral deconjugases in immune evasion
iv) Virus mediated Ub and UbL modifications
v) Methods to study Ub and UbL modifications during virus infection
vi) Novel antiviral targets in the ubiquitin system
