New research identifies a key factor that defines herpes virus progression and reveals that targeting it can slow viral progression.
According to the latest statistics from the Centers for Disease Control and Prevention (CDC), about 48 percent of people identified with herpes simplex 1 in the United States in 2015–2016, a viral strain that causes oral infections.
80 percent of the population worldwide have the virus. The virus never goes away once a person contracts it — it remains dormant throughout their life in their body.
Although symptoms of herpes sometimes go unnoticed, they may be unpleasant and painful for some people.
Also highly contagious is the herpes virus, as a person can pass it on even if they have no symptoms.
New research suggests that contracting the virus could soon be preventable as scientists provide new insights into what is happening at the cellular level during an infection with herpes and find a way to slow the progression of the infection.
Emanuel Wyler, Ph.D., and Vedran Franke, Ph.D., of the Berlin Institute for Medical Systems Biology, Germany, are the co-leading authors of the new paper published in Nature Communications.
The scientists developed an algorithm that enabled them to predict how individual cells will develop an infection.
Researchers analyzed 12,000 human skin cells infected with herpes simplex virus 1 (HSV1) using single-cell RNA sequencing. Single cell RNA sequencing is a revolutionary technique that allows for the breakdown of genetic expressions at a much more granular level than bulk RNA sequencing.
Researchers use a smoothie analogy to explain the difference between single-cell RNA sequencing and conventional, bulk RNA sequencing.
“If I put ten fruit types in a blender, I can say roughly that when I taste it, the smoothie contains, say, blackberries,” explains Wyler. “We’re not making a smoothie with single-cell RNA sequencing — we’re making a fruit salad. I can immediately identify the blackberries and say exactly how many are in the salad.”
Combined with the algorithm, the methodology revealed to the researchers that a transcription factor called NRF2 plays a key role in preventing the progression of the infection.
Transcription factors are proteins that “decode” information from our genome and by binding to certain DNA regions, activate or deactivate specific genes.
Franke discusses how the NRF2 transcription factor was revealed by the new technique.
“I saw changes in the regulation of each gene that we were investigating in a single cell,” he says. “This showed us that the NRF2 transcription factor’s activation level can be a marker for temporary HSV1 resistance.”
The researchers have found that two agonists or activators of NRF2 called bardoxolone methyl and sulforaphane inhibit the virus’s production that is, make the virus activate less of its own genes. This confirmed NRF2’s key role for the researchers.
Bardoxolone methyl is a medicine for chronic infection of the kidney. It is currently in its third phase of clinical trials.
Eventually, the study also revealed that the cell cycle stage also affects the susceptibility of a cell to HSV1 infection.
The researchers demonstrate that the herpes virus is a good “general blueprint” for studying viral infection cell states, and they plan to use single-cell RNA sequencing to research future viruses.


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