A recent study published in Nature Communications reveals that the herpes simplex virus-1 (HSV-1) can rearrange the DNA structure in human cells shortly after infection, allowing it to access essential host genes more effectively.

Dr. Esther González Almela, the first author of the study, describes HSV-1 as an 'opportunistic interior designer' that manipulates the human genome to exploit host resources for its replication.

Blocking the enzyme topoisomerase I in the host cell prevents HSV-1 from rearranging the host genome and stops the production of new viral particles, highlighting potential avenues for antiviral development.

The complete inhibition of TOP1 expression halted HSV-1 infection, although current TOP inhibitors do not specifically target the virus.

Researchers utilized advanced imaging techniques to observe significant changes in cellular DNA within just eight hours of HSV-1 infection, demonstrating that the virus alters the shape and compactness of host chromosomes.

By the third hour of infection, HSV-1 had utilized topoisomerase I and cohesin, leading to a 30% compaction of the DNA's volume and a notable reduction in the transcription of human genes.

Within the first hour of infection, HSV-1 co-opts key host genes, including RNA polymerase II and DNA topoisomerase, which contribute to the condensation of the host's chromatin into dense bundles.

The microscopy technique STORM-PAINT used in this research allows for high-resolution imaging of DNA molecules, enhancing our understanding of how viruses manipulate host chromatin.

This research could pave the way for new treatments targeting HSV-1 infections, which affect a significant portion of the population.

Approximately two-thirds of individuals are estimated to carry HSV-1, often asymptomatically, but it can lead to serious complications such as cold sores and blindness in vulnerable populations.

The findings raise new questions about the relationship between chromatin organization and function, with implications for understanding both viral strategies and the complexities of the human genome.

This study challenges previous assumptions that dense chromatin solely shuts down genes, suggesting a more intricate relationship between transcription activity and DNA structure.