In the intricate battle against viral infections, the host’s immune system relies heavily on cytokine signaling pathways to mount an effective response. These signaling pathways are crucial for coordinating the innate immune response, which involves various cytokines and receptors working together to recognize, limit, and eliminate viral threats. For example, innate immune sensors (TLRs, RIG-I/MDA5, cGAS etc.) recognize RNA or DNA viruses and then recruit downstream key patterners to activate IFN and NF-?B, respectively, resulting in the production of type I IFN, immune-stimulated genes (ISGs), cytokines and restriction factors. Also, Autophagy, apoptosis, pyroptosis or necroptosis could also be activated during viral infection. Despite these defense mechanisms, many viruses have evolved sophisticated strategies to evade detection and suppression by the host immune system, complicating effective treatment and management of infections. For example, the ubiquitin-specific protease (UL36) and UL24 of HSV-1, antagonize the cGAS–STING-mediated NF-?B pathway via different mechanisms. The former restricts I?Ba degradation dependent on its deubiquitinates activity, and the latter interacts with the NF-?B subunits p65 and p50 to reduce their nuclear translocation. Interestingly, SARS-CoV-2 ORF3a is a multitask protein which targets cGAS-STING-NF-kB and autophagy axis. PSGL-1 is induced by interferon-? in activated CD4+T cells to inhibit HIV-1 reverse transcription and potently block viral infectivity by incorporating in progeny virions. However, this infective block is antagonized by HIV-1 Vpu via PSGL-1 degradation. Understanding the complex interactions between cytokine signaling and viral evasion is essential to developing new therapeutic strategies.
The goal of this Research Topic is to investigate the intricate interplay between cytokine signaling pathways and innate immune responses in the modulation of viral infections, with a specific focus on how viruses evade these immune defenses. By delving into the mechanisms through which pathway including various innate immune sensing or cell death processes, influence immune cell function and viral replication, and exploring viral strategies for immune evasion, this topic aims to enhance our understanding of host-pathogen interactions. Ultimately, this research will identify novel therapeutic strategies for combating viral infections, contributing to developing more effective treatments and preventive measures.
This Research Topic aims to explore the role of cytokine signaling pathways and innate immune responses in modulating viral infections and the mechanisms viruses employ to evade these defenses. We seek contributions addressing the following areas: Investigating the roles of cytokines (interferons, tumor necrosis factors, interleukins) in viral infections, their influence on immune cell function, host cell states, and viral replication.
1. Examining the roles of innate immune pathways (RLR, TLR, cGAS-STING) and cells (natural killer cells, macrophages, dendritic cells) in identifying and eliminating viruses, and the regulation of their interactions.
2. Exploring mechanisms by which viruses evade host immune surveillance, disrupt cytokine signaling, suppress immune responses, and adapt to immune pressures, along with specific viral strategies for immune evasion.
3. Presenting recent advances in gene editing, vaccine development, and immune modulation therapies, and assessing the potential and challenges of these approaches in treating viral infections.
In the intricate battle against viral infections, the host’s immune system relies heavily on cytokine signaling pathways to mount an effective response. These signaling pathways are crucial for coordinating the innate immune response, which involves various cytokines and receptors working together to recognize, limit, and eliminate viral threats. For example, innate immune sensors (TLRs, RIG-I/MDA5, cGAS etc.) recognize RNA or DNA viruses and then recruit downstream key patterners to activate IFN and NF-?B, respectively, resulting in the production of type I IFN, immune-stimulated genes (ISGs), cytokines and restriction factors. Also, Autophagy, apoptosis, pyroptosis or necroptosis could also be activated during viral infection. Despite these defense mechanisms, many viruses have evolved sophisticated strategies to evade detection and suppression by the host immune system, complicating effective treatment and management of infections. For example, the ubiquitin-specific protease (UL36) and UL24 of HSV-1, antagonize the cGAS–STING-mediated NF-?B pathway via different mechanisms. The former restricts I?Ba degradation dependent on its deubiquitinates activity, and the latter interacts with the NF-?B subunits p65 and p50 to reduce their nuclear translocation. Interestingly, SARS-CoV-2 ORF3a is a multitask protein which targets cGAS-STING-NF-kB and autophagy axis. PSGL-1 is induced by interferon-? in activated CD4+T cells to inhibit HIV-1 reverse transcription and potently block viral infectivity by incorporating in progeny virions. However, this infective block is antagonized by HIV-1 Vpu via PSGL-1 degradation. Understanding the complex interactions between cytokine signaling and viral evasion is essential to developing new therapeutic strategies.
The goal of this Research Topic is to investigate the intricate interplay between cytokine signaling pathways and innate immune responses in the modulation of viral infections, with a specific focus on how viruses evade these immune defenses. By delving into the mechanisms through which pathway including various innate immune sensing or cell death processes, influence immune cell function and viral replication, and exploring viral strategies for immune evasion, this topic aims to enhance our understanding of host-pathogen interactions. Ultimately, this research will identify novel therapeutic strategies for combating viral infections, contributing to developing more effective treatments and preventive measures.
This Research Topic aims to explore the role of cytokine signaling pathways and innate immune responses in modulating viral infections and the mechanisms viruses employ to evade these defenses. We seek contributions addressing the following areas: Investigating the roles of cytokines (interferons, tumor necrosis factors, interleukins) in viral infections, their influence on immune cell function, host cell states, and viral replication.
1. Examining the roles of innate immune pathways (RLR, TLR, cGAS-STING) and cells (natural killer cells, macrophages, dendritic cells) in identifying and eliminating viruses, and the regulation of their interactions.
2. Exploring mechanisms by which viruses evade host immune surveillance, disrupt cytokine signaling, suppress immune responses, and adapt to immune pressures, along with specific viral strategies for immune evasion.
3. Presenting recent advances in gene editing, vaccine development, and immune modulation therapies, and assessing the potential and challenges of these approaches in treating viral infections.