Chandelier
Senior Member (Voting Rights)
Frontiers | Epigenetic Regulation in Persistent, Latent, Oncogenic, and Selected Post-Acute Viral Infections
Viruses have evolved sophisticated strategies to modulate host epigenetic machinery, enabling viral persistence, immune evasion, latency, reactivation, and, ...
www.frontiersin.org
Submission deadlines
- Manuscript Submission Deadline 27 February 2027
Background
Viruses have evolved sophisticated strategies to modulate host epigenetic machinery, enabling viral persistence, immune evasion, latency, reactivation, and, in some cases, oncogenesis. These mechanisms are best characterized in chronic, latent, and oncogenic viruses, including herpesviruses (like HSV, CMV, EBV, KSHV, HHV-6), HIV, HBV, and HPV, where chromatin remodelling, DNA and histone modifications, viral non-coding RNAs, and host-virus transcriptional control are central to latency, reactivation, immune evasion, and tumorigenesis. Despite this progress, key mechanistic questions remain about how viral factors reshape host chromatin and how host cells deploy epigenetic defences in return.At the same time, the role of epigenetic regulation in acute and post-acute viral infections remains less clearly defined. In many acute infections, observed epigenetic changes may be transient, cell-type specific, or secondary to inflammation rather than direct viral epigenetic reprogramming. However, emerging evidence suggests that selected viral infections may leave longer-lasting epigenetic imprints on host cells, including changes in chromatin accessibility, innate immune signalling thresholds, metabolic programs, and trained immune responses. These processes may be relevant to post-acute viral diseases such as Long COVID, ME/CFS, and related post-viral chronic conditions, although causal relationships and clinical impact remain under active investigation.
This Research Topic aims to examine how persistent, latent, oncogenic, and selected post-acute viral infections interact with the host epigenetic landscape, how these interactions contribute to viral persistence, immune regulation, pathogenesis, and chronic host-cell states, and whether aberrant epigenetic changes can be therapeutically reversed. We particularly welcome studies that integrate molecular virology, epigenetics, immunology, systems biology, and clinically relevant models to advance a rigorous understanding of host–virus epigenetic crosstalk.
We invite contributions addressing, but not limited to:
1. Epigenetic mechanisms in persistent, latent, and oncogenic viral infections, including chromatin remodelling, DNA/RNA methylation, histone modifications, and viral or host factors regulating latency, reactivation, persistence, immune evasion, and oncogenesis.
2. Host–virus transcriptional and epigenetic networks, including the roles of viral non-coding RNAs, viral proteins, host chromatin regulators, and epigenetic defense mechanisms in controlling viral and host gene expression.
3. Epigenetic immune memory and trained immunity in selected post-acute viral settings, including Long COVID, ME/CFS, and related post-infection syndromes, especially studies that can contribute mechanistic evidence to any clinical association.
4. Single-cell, spatial, and multi-omics approaches that reveal dynamic, cell-type-specific epigenetic changes during viral infection, persistence, latency, reactivation, or post-acute immune dysregulation, preferably with functional or independent validation.
5. Therapeutic and translational approaches, including small-molecule epigenetic modulators, CRISPR-based epigenome editing, antiviral-epigenetic combination strategies, and interventions aimed at reversing maladaptive host-cell states.
Article types and fees
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:- Editorial
- FAIR² Data
- FAIR² DATA Direct Submission
- Hypothesis and Theory
- Methods
- Mini Review
- Opinion
- Original Research
- Perspective
- Review
- Systematic Review
- Technology and Code