About this Research Topic
Interferon-induced proteins play pivotal roles in the immune response against viral infections, acting through diverse mechanisms. These proteins form the first line of defense in antiviral immunity by engaging in complex interactions with co-factor proteins or sometimes with cellular protein degradation systems, including ubiquitin-proteasome pathway and autophagy-lysosome pathway. Moreover, some interferon-induced proteins may directly bind to viral factors and exert their antiviral effects through de novo host-virus interactions. The intricate molecular pathways through which these proteins operate are crucial but not yet fully understood, representing significant gaps in current research, especially in terms of their potential as therapeutic targets.
This Research Topic aims to deepen our understanding of interferon-stimulated proteins, and their mechanistic roles in combating viral infections. It seeks to elucidate the molecular mechanisms of their antiviral defense, aiming to identify innovative therapeutic targets that could enhance antiviral defenses.
In pursuit of clarity and progress within this field, our focus will narrow to key research areas requiring thorough investigation. We aim to extend our knowledge on the cellular mechanisms and pathways involving these proteins.
• Detailed functional analysis of interferon-induced proteins in viral defense (e.g. PKR, OAS and RNase L, ISG15 or other ISG proteins, Mx proteins, IFITMs, viperin, IDO1, FAT10, GILT, BST2/tetherin, ZAPs)
• Mapping of molecular pathways facilitated by these proteins
• Exploration of potential antiviral therapeutic applications
• Comparative studies across different viral infections to discern common and unique mechanisms
• Identification of new interferon-induced proteins that inhibit viral replication and/or alter host cell homeostasis
• Regulation mechanism of their expression in the signal cascade stimulated by interferons under physiological microenvironment
• Contribution of interferon-induced proteins in protection against viral pathogenesis
Through examining these aspects, we anticipate generating impactful insights into the antiviral capacities of interferon-induced proteins and their potential exploitation in medical therapies.
This Research Topic aims to deepen our understanding of interferon-stimulated proteins, and their mechanistic roles in combating viral infections. It seeks to elucidate the molecular mechanisms of their antiviral defense, aiming to identify innovative therapeutic targets that could enhance antiviral defenses.
In pursuit of clarity and progress within this field, our focus will narrow to key research areas requiring thorough investigation. We aim to extend our knowledge on the cellular mechanisms and pathways involving these proteins.
• Detailed functional analysis of interferon-induced proteins in viral defense (e.g. PKR, OAS and RNase L, ISG15 or other ISG proteins, Mx proteins, IFITMs, viperin, IDO1, FAT10, GILT, BST2/tetherin, ZAPs)
• Mapping of molecular pathways facilitated by these proteins
• Exploration of potential antiviral therapeutic applications
• Comparative studies across different viral infections to discern common and unique mechanisms
• Identification of new interferon-induced proteins that inhibit viral replication and/or alter host cell homeostasis
• Regulation mechanism of their expression in the signal cascade stimulated by interferons under physiological microenvironment
• Contribution of interferon-induced proteins in protection against viral pathogenesis
Through examining these aspects, we anticipate generating impactful insights into the antiviral capacities of interferon-induced proteins and their potential exploitation in medical therapies.
Keywords: Interferon-stimulated proteins, IDO1, Autophagy, Viral infections, Therapeutic targets
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
