by The cold, painful herpes simplex virus (HSV-1) takes human cells and reconfigures its DNA within one hour after the infection, according to a new study that could help combat the pathogen.
Viruses depend on their hosts for replication, and when they infect cells, they tend to take over their cellular machines to make new copies of themselves.
Scientists have now found that the Herpes virus not only kidnaps the genome of its host, but also reorganized the entire internal structure of the cells within one hour after the infection.
Two out of three people under the age of 50 live with HSV-1 and have the virus for life after infecting.
Although most cases manifest asymptomatic or as most benign but recurring fever blister, the virus can in rare cases cause blindness or life -threatening illness in rare cases.
Recent studies also suggest that there could be a connection between herpes infection and dementia in older adults.
The new study published in the journal Natural communication, found that HSV-1 turns the structure of the human genome and makes it compact and tight so that the virus can access host genes that are most useful to reproduce.
This finding could lead to new treatments to control the virus, which is infected by almost four billion people worldwide.
“HSV-1 is an opportunistic interior designer who redesigned the human genome with great precision and decides which parts it come into contact with. It is a new mechanism of manipulation, of which we did not know that the virus had to take advantage of the host’s resources,” said Esther González Almela, first author of the study.
While earlier studies have pointed out that an HSV infection leads to compact and redesigned host chromosomes, it remained unclear whether it was a side effect of the infection with cold sore virus infection or was caused directly by the pathogen itself.
The most recent study is the first to prove that HSV-1 intentionally and within a few hours after infection.
The researchers also found that the blocking of a single host cell enzyme – topoisomerase I – completely blocked the decisive ability of the cold virus to reorganize the human genome.
“In cell culture, inhibiting this enzyme stopped the infection before the virus could make a single new particle,” said Pia Cosma, another author of the study.
“This gives us a potential new therapeutic goal to stop the infection,” said Dr. Cosma.
In the study, scientists used super-resolution microscopy to fit only 20 nanometers wide in ultra-small cell structures, which is about 3,500 times thinner than a hairline.
They combined this with a different technique that shows which DNA parts touch.
These techniques showed that the enemy takeover of the herpes virus begins within the very beginning, with the virus an important human enzyme-RNA polymerase II, in order to synthesize its own proteins.
Just three hours after the infection, the virus causes a considerable part of molecules that are involved in the human DNA replication to give up the cell nucleus and enter viral replication compartments.
The theft wholesale leads to a collapse of every activity in the entire host genome, which is then only broken down into a dense shell.
Scientists hope that the latest knowledge due to its prevalence and ability to cause recurring outbreaks can cope with the global challenge of the global health challenge.
