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Herpes Simplex Virus Reshapes Human Genome, Scientists Find
The common virus responsible for cold sores, herpes simplex virus type 1 (HSV-1), rapidly alters our genetic code. Within an hour of infection, it manipulates the genome to accelerate its propagation. Scientists believe this discovery could potentially lead to innovative treatments for severe cases. Understanding this process provides valuable insights into combating the virus.
Billions globally are infected with herpes simplex virus type 1 (HSV-1), though many remain unaware. Transmission occurs via contact with cold sores, saliva, or unbroken skin surrounding the mouth.
Upon infiltrating host cells, the virus duplicates in the nucleus, the repository of DNA. This genetic material exists as strands intertwined with proteins. Certain regions form tight coils, deactivating genes, whereas others manifest as expanded loops where genes are active. Transcription proteins can access these looser regions, converting DNA to RNA, which produces proteins for cellular function.
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Previous research indicates that the human genome tightens during HSV-1 infection, potentially disrupting cellular functions, but the cause of this phenomenon was unclear.
Unveiling the Viral Mechanism
To investigate, Alvaro Castells-Garcia and colleagues at the Centre for Genomic Regulation in Barcelona, Spain, utilized advanced microscopy to visualize HSV-1 infecting human lung cells. The microscope facilitated observation of structures 3500 times finer than a strand of hair. “It represents a higher level of detail than previous investigations,” stated Castells-Garcia.
The team observed that within one hour of viral entry, the virus sequestered transcription proteins from the human genome, confirming previous findings.
This sequestration appears to trigger the host DNA to compress, reducing to 30% of its original volume within eight hours post-infection.
Targeting Key Genomic Regions
The virus also interacts with specific host genome areas responsible for producing the hijacked transcription proteins. This interaction inhibits coiling in these regions, augmenting the activity of growth-promoting viral genes.
“Previously, we thought the interaction with our genome was random,” explained Esther González-Almela, a team member at the Centre for Genomic Regulation. “However, the virus can target specific regions involved in sustaining infection, making viral RNA and proteins.”
Potential Therapeutic Interventions
Another facet of the study involved using an experimental cancer drug to inhibit the transcription protein HSV-1 hijacks. This intervention prevented viral replication in human lung cells in the laboratory setting. González-Almela suggests that the drug may prove valuable in treating severe cold sores or immunocompromised individuals at risk of complications. Generally, mild cases resolve without intervention.
Broader Implications
The findings could extend to other viruses, such as adenoviruses (common cold) and varicella-zoster virus (chickenpox). Benjamin Krishna at the University of Cambridge noted, “If other viruses similar to HSV-1 employ identical strategies, these experimental drugs might offer therapeutic benefits.”
Key Takeaways:
- HSV-1 swiftly reshapes the human genome upon infection.
- The virus steals transcription proteins, causing DNA to coil tightly.
- Targeting these mechanisms may offer novel treatment avenues.