Viruses come in many forms and sizes, with genomes of very diverse nature and complexity. Besides this variability, all viruses are obligated parasites. This means that to complete their life cycle, they need to hijack cellular components for their own use. For example, viruses utilize plasma membrane proteins to attach to the cell surface, the microtubule network to travel through the cytoplasm, and even antibodies to enhance the infection. Nevertheless, cells have also evolved mechanisms to counteract viral infection by means of specific proteins able to inhibit virus replication, such as interferon stimulated genes (ISGs). The tug-of-war established between this opposite forces ultimately defines the fate of the infection.
Our current knowledge on the way viruses reprogram the cell for their advantage, and the cellular countermeasures to inhibit infection is incomplete. However, understanding the delicate balance between viral restriction factors and cofactors existing within the infected cell is pivotal for the development of new therapeutic strategies. Therefore, advances in antiviral drug design have resulted in viral inhibitors targeting cellular components, such as the cyclophilin A inhibitor cyclosporine, for influenza A virus (IAV), or monoclonal antibodies against anti-occludin and anti-claudin-1 for hepatitis C virus (HCV). Inhibiting the cellular machinery employed by the virus during replication does not only increase the arsenal available to fight the infection but has the advantage of the low mutation propensity of these proteins. This is an improvement over classical antiviral drugs targeting viral components, which frequently lead to mutation of the target protein and virus resistance. In addition, understanding the inhibitory mechanism of viral restriction factors could inform of unknown vulnerabilities during the virus life cycle.
This research topic aims to attract attention to the complex interplay between viral infection and the host factors facilitating or inhibiting virus replication. We welcome original research articles, reviews, methods, case reports and opinions from a broad range of disciplines. This includes, but is not limited to:
- The role of cellular proteins on the pathogenesis of RNA and DNA viruses.
- The development/validation of antiviral strategies based on this interaction, including bioinformatic approaches, clinical trials, or drug design studies.
- The evolution of viral countermeasures to escape inhibition by cellular restriction factors.
Viruses come in many forms and sizes, with genomes of very diverse nature and complexity. Besides this variability, all viruses are obligated parasites. This means that to complete their life cycle, they need to hijack cellular components for their own use. For example, viruses utilize plasma membrane proteins to attach to the cell surface, the microtubule network to travel through the cytoplasm, and even antibodies to enhance the infection. Nevertheless, cells have also evolved mechanisms to counteract viral infection by means of specific proteins able to inhibit virus replication, such as interferon stimulated genes (ISGs). The tug-of-war established between this opposite forces ultimately defines the fate of the infection.
Our current knowledge on the way viruses reprogram the cell for their advantage, and the cellular countermeasures to inhibit infection is incomplete. However, understanding the delicate balance between viral restriction factors and cofactors existing within the infected cell is pivotal for the development of new therapeutic strategies. Therefore, advances in antiviral drug design have resulted in viral inhibitors targeting cellular components, such as the cyclophilin A inhibitor cyclosporine, for influenza A virus (IAV), or monoclonal antibodies against anti-occludin and anti-claudin-1 for hepatitis C virus (HCV). Inhibiting the cellular machinery employed by the virus during replication does not only increase the arsenal available to fight the infection but has the advantage of the low mutation propensity of these proteins. This is an improvement over classical antiviral drugs targeting viral components, which frequently lead to mutation of the target protein and virus resistance. In addition, understanding the inhibitory mechanism of viral restriction factors could inform of unknown vulnerabilities during the virus life cycle.
This research topic aims to attract attention to the complex interplay between viral infection and the host factors facilitating or inhibiting virus replication. We welcome original research articles, reviews, methods, case reports and opinions from a broad range of disciplines. This includes, but is not limited to:
- The role of cellular proteins on the pathogenesis of RNA and DNA viruses.
- The development/validation of antiviral strategies based on this interaction, including bioinformatic approaches, clinical trials, or drug design studies.
- The evolution of viral countermeasures to escape inhibition by cellular restriction factors.
