Authors
Panagiotis Keramidas, Maria Pitou, Amalia Aggeli, Sotiris Varlamis, Theodora Choli-Papadopoulou
Published in
The FEBS journal. Oct 13, 2026. Epub Oct 13, 2026.
Abstract
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.
PMID:
42867253
Bibliographic data and abstract were imported from PubMed on 14 Oct 2026.
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