A chimeric infection program and epigenetic conflict underpin endogenous giant virus latency
- 1Virginia Tech
Abstract
Giant endogenous viral elements (GEVEs) are ubiquitous in eukaryotic genomes, but how the virus adapts to the host and is capable of reactivation despite host defense mechanisms remains unclear. Here we examined this process in the green alga Chlamydomonas reinhardtii and its latent giant virus, punuivirus, which is integrated into the host genome. We reveal a chimeric genomic architecture in which punuivirus latency genes are enriched in spliceosomal introns and 6-methyladenine marks, mirroring host transcriptional regulation, while virulence genes are predominantly controlled by a conserved viral promoter. Using single-cell RNA-seq, we show that nearly 70% of cells express viral transcripts, but only a small subpopulation commits to viral production, expressing virulence genes with host transcriptional shutoff. Moreover, we find that the intact punuivirus GEVE remains refractory to host 5-methylcytosine (5mC) silencing, whereas a naturally occurring deletion variant is associated with widespread 5mC accumulation across the GEVE and elsewhere in the host genome. The deleted region encodes a highly expressed ten-eleven translocation dioxygenase (TET), and epigenetic profiling of intact and deletion strains implicates this GEVE gene in removing 5mC marks, thereby maintaining the virus in a transcriptionally permissive latent state. Our study provides novel insights into the molecular underpinnings of host-virus co-existence in a giant virus-alga interaction.
Related
- Engineered Chimeric Proteins Functionally Replace ALS-causing Endogenous FUS and TDP-43 to Improve Neuronal Health
- Arsenic Resistance Protein BcArs2 Modulates Endogenous ROS Homeostasis in Infection Cushions to Enhance the Virulence of Botrytis cinerea Toward Host Plants
- Latent endogenous giant viruses drive active infection and inheritance in a multicellular algal host
- Identifying Hemodialysis Patients With the Highest Risk of Staphylococcus aureus Endogenous Infection Through a Simple Nasal Sampling Algorithm
- Cortex-wide neuronal dynamics underpin quasi-periodic patterns in resting-state fMRI
BibTeX
@misc{sheyn2026chimeric,
title = {{A chimeric infection program and epigenetic conflict underpin endogenous giant virus latency}},
author = {U. Sheyn and R. Heery and M. P. Erazo-Garcia and L. Xu and R. J. Craig and A. de Mendoza and F. Aylward},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.09.758095},
url = {https://www.biorxiv.org/content/10.64898/2026.10.09.758095v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - A chimeric infection program and epigenetic conflict underpin endogenous giant virus latency
AU - U. Sheyn
AU - R. Heery
AU - M. P. Erazo-Garcia
AU - L. Xu
AU - R. J. Craig
AU - A. de Mendoza
AU - F. Aylward
PY - 2026
DA - 2026/10/09
PB - bioRxiv
DO - 10.64898/2026.10.09.758095
UR - https://www.biorxiv.org/content/10.64898/2026.10.09.758095v1
AB - Giant endogenous viral elements (GEVEs) are ubiquitous in eukaryotic genomes, but how the virus adapts to the host and is capable of reactivation despite host defense mechanisms remains unclear. Here we examined this process in the green alga Chlamydomonas reinhardtii and its latent giant virus, punuivirus, which is integrated into the host genome. We reveal a chimeric genomic architecture in which punuivirus latency genes are enriched in spliceosomal introns and 6-methyladenine marks, mirroring host transcriptional regulation, while virulence genes are predominantly controlled by a conserved viral promoter. Using single-cell RNA-seq, we show that nearly 70% of cells express viral transcripts, but only a small subpopulation commits to viral production, expressing virulence genes with host transcriptional shutoff. Moreover, we find that the intact punuivirus GEVE remains refractory to host 5-methylcytosine (5mC) silencing, whereas a naturally occurring deletion variant is associated with widespread 5mC accumulation across the GEVE and elsewhere in the host genome. The deleted region encodes a highly expressed ten-eleven translocation dioxygenase (TET), and epigenetic profiling of intact and deletion strains implicates this GEVE gene in removing 5mC marks, thereby maintaining the virus in a transcriptionally permissive latent state. Our study provides novel insights into the molecular underpinnings of host-virus co-existence in a giant virus-alga interaction.
ER -