Ariza et al. (2025)
- Authors: Maria Eugenia Ariza, Irene Mena Palomo, Marshall V. Williams
- Institutes: Department of Cancer Biology and Genetics, The Ohio State University College of Medicine, Columbus, OH, USA, Institute for Behavioral Medicine Research, The Ohio State University College of Medicine, Columbus, OH, USA
- Publisher: Viruses
- Link: DOI
Summary
This research shifts the focus from finding a single “guilty” virus to understanding how a “team” of common, dormant herpesviruses can collaborate to cause chronic illness. By identifying a specific “zombie” state of viral activity, it explains why current tests often come back negative despite severe symptoms and points toward more effective, multi-targeted treatment strategies. This model provides a scientific basis for why many patients experience a sudden onset after a new infection, like COVID-19, which acts as a master switch for these dormant viruses.
What was researched?
The study investigates whether ME/CFS and Long COVID are driven by the simultaneous “abortive lytic replication” of multiple human herpesviruses rather than a single active infection.
Why was it researched?
It was researched to address why no single etiological agent has been found and why traditional antiviral treatments, which focus on full viral replication, often produce inconsistent clinical results.
How was it researched?
This is a comprehensive hypothesis-driven literature review that synthesizes findings from over 200 references, focusing on the molecular biology of herpesviruses and the immune responses of ME/CFS patients.
What has been found?
The authors found that multiple herpesviruses, such as EBV and HHV-6, can enter a “partially awake” state where they produce toxic proteins like dUTPase without completing a full infection cycle. These proteins act as chronic triggers for the immune system, leading to sustained inflammation and the characteristic symptoms of the disease even when viral loads appear low.
Discussion
The paper discusses how a secondary trigger, like COVID-19, might act as a master switch to reactivate several dormant viruses at once. It also highlights the limitations of current diagnostic methods that only look for full viral replication (lytic) or total dormancy (latent), effectively missing the problematic intermediate state.
Conclusion & Future Work
The authors conclude that ME/CFS is likely a poly-herpesvirus mediated disease. They suggest that future research and treatments should focus on markers of abortive replication and substances like valganciclovir 💊 that have shown potential in specific patient subsets.