Human DNA within cells in its natural state (left) contrasted with its state eight hours after cold sore virus infection (right)
Esther Gonzalez Almera and Alvaro Castells Garcia
Viruses that typically cause herpes can reform their genome within an hour following infection, potentially allowing scientists to address severe cases more effectively.
Billions globally are infected by Herpes Simplex Virus Type 1 (HSV-1), often without their knowledge. Transmission occurs via contact with infected saliva or skin around the mouth.
Upon invading a host cell, the virus replicates within the nucleus, where genetic material is preserved among the strands of DNA. These strands surround proteins, with some sections tightly coiling to deactivate genes while others form looser loops where genes remain active. In these less dense areas, proteins can transcribe DNA into messenger RNA, encoding for a protein essential for cellular function.
Prior research has indicated that the human genome becomes more tightly coiled following HSV-1 infection, possibly disrupting cellular functions, although the cause of this coiling was previously uncertain.
For further details, consult Alvaro Castells-Garcia at the genome regulatory center in Barcelona, Spain, whose team employs advanced microscopy to investigate HSV-1, infecting human lung cells and observing structures that are 3,500 times thinner than a hair. “This offers a higher resolution than most prior studies,” notes Castells-Garcia.
They discovered that within an hour post-infection, transcription factors were already pilfered from the human genome, corroborating previous findings.
Moreover, this thievery is what appears to cause the host’s DNA to coil more tightly, compressing it to 30% of its volume within 8 hours of infection.
The virus also interacts with specific areas of the host genome that encode the stolen transcription factors, inhibiting activity in those regions and enhancing the expression of genes that facilitate its own growth.
“Previously, I thought the virus made random contacts with the genome,” comments team member Esther Gonzalez Almera at the genome regulation center. “However, it’s clear that viruses specifically target certain regions of their genome, which often contain genes critical to sustaining the infection and producing viral RNA and proteins.”
In another segment of the study, researchers found that utilizing experimental cancer treatments to obstruct one of the transcription factors taken by HSV-1 inhibited its replication in human lung cells in the laboratory. This suggests that such medications could assist in treating HSV-1 in individuals suffering from severe herpes outbreaks and those at higher risk for complications, as González-Almela explains. Mild cases typically resolve without intervention.
This treatment may also be effective against other pathogens, such as adenoviruses that lead to colds, and noroviruses associated with gastroenteritis. “Other viruses similar to HSV-1 may employ analogous strategies,” states Benjamin Krishna from Cambridge University. “These could represent [potential types of experimental drugs] for addressing such cases as well,” he adds.
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Source: www.newscientist.com
