Dr. Esther González Almela describes HSV-1 as an 'opportunistic interior designer' that intentionally rewires DNA contacts to create an optimal environment for its multiplication.

An experimental cancer drug that blocks one of the transcription proteins stolen by HSV-1 has shown promise in laboratory settings for preventing viral replication, suggesting potential treatment options for severe HSV-1 cases.

The findings of this study suggest that similar strategies may apply to other viruses, such as adenoviruses and varicella zoster virus, opening avenues for broader antiviral treatments.

A recent study published in Nature Communications reveals that the herpes simplex virus type 1 (HSV-1), known for causing cold sores, begins altering the human genome within an hour of infection to enhance its replication.

The virus specifically targets genomic regions that encode transcription proteins, preventing coiling in those areas and promoting gene activity that is essential for its growth.

To facilitate its replication, HSV-1 employs topoisomerase I (TOP1) and cohesin to form viral replication compartments (VRCs), which significantly slow human transcription and compact chromatin by 70%.

As these VRCs expand, human DNA is pushed to the edges of the nucleus, resulting in a dramatic decrease in human gene activity and a surge in viral RNA production.

Shortly after invading host cells, HSV-1 hijacks the host's RNA polymerase II (RNAP II), redirecting it from producing human RNA to replicating its own viral genes.

Research led by Alvaro Castells-Garcia indicates that HSV-1 steals transcription proteins from the human genome, causing the host DNA to coil tighter and shrink significantly within eight hours of infection.

Interestingly, HSV-1 does not alter chemical markers on DNA; instead, it modifies the physical structure and positioning of the DNA itself, challenging previous assumptions about gene regulation.

Despite these extensive changes, some regions of the human genome maintain their structural integrity, indicating that chromatin can resist viral manipulation.

Blocking the host enzyme TOP1 completely prevents the virus from reshaping the genome, presenting a potential therapeutic target for HSV-1, which affects nearly two-thirds of individuals under 50.