A comparative analysis of cell death signalling in RNA and DNA virus infections and potential inhibitory strategies.

The recent COVID-19 pandemic and the epidemic outbreak of Mpox have demonstrated that viruses, despite their apparently simple structure, are sophisticated microorganisms that have evolved complicated pro-survival mechanisms. Their potential to manipulate cell death pathways can affect and determine the outcome of the infection cycle and the host's immune response. RNA viruses typically display a more acute and aggressive nature, as they often promote cell death. In this way, they proliferate and release their virions to infect adjacent cells and perpetuate their life cycle. Common consequences of RNA virus infection include hyperinflammatory responses in hosts, typically leading in damage to the epithelial barrier. Conversely, DNA viruses modulate these pathways to sustain a balance between the lytic cycle, during which they replicate, and latency, wherein they remain inactive until an appropriate stimulus triggers reactivation. Achieving this balance and transitioning between stages of infection requires the inhibition of cellular death processes. In both instances, the viruses seem to respond to the cellular context, enhancing their adaptability through mutations, so to deceive host defenses and therefore secure their survival. This highlights the necessity to comprehend the processes via which these biological threats induce cell death, thereby facilitating the development of broad-spectrum or targeted antiviral treatments.