In what could be a breakthrough for treating shingles, Israeli scientists have created a stable state of dormant herpes in nerve cells grown in the lab. They also managed to reawaken the "sleeping" virus under controlled conditions, a scientific first.
The new understandings gained into the virus' behavior through this ground-breaking model could lead to new generations of drugs to treat herpes zoster, also known as shingles.
Creating a lab model is a good thing because unlike the herpes on your leg, for instance, cells in a petri dish can be experimented with. And although the disease is extremely common, to say the least, much about it remains unknown.
The breakthrough model developed by scientists at Bar-Ilan University is the first to mimic the dormant/active behavior of varicella zoster virus, or VZV – the virus that causes chicken pox, and after that, the maddening condition known as shingles that can develop even decades after the initial infection.
A sleeping danger
A third of the people on the planet are believed to carry VZV. For most, the pain of the rash passes within days or weeks. For some, it can last years. That is because we may overcome the chicken pox itself, but the virus remains "asleep" in our nerve cells.
The molecular mechanism that causes the virus to wake up and torment us with shingles vesicles is unknown, though it is clear that not only weakened immune reactions but even an emotional jolt can be triggers.
But perhaps those molecular mechanisms can be elucidated now that scientists at Bar-Ilan University have managed to achieve a state of dormant infection in human neurons (nerve cells) grown in petri dishes from embryonic stem cells.
The more we know about the molecular mechanisms of herpes awakening, the better equipped we will be to developed drugs to stop it in its molecular tracks.
The model isn't an exact emulation of our human reality. We can host the dormant virus forever. At this point, the lab has hosted dormant VZV in nerve cells in a petri dish for seven weeks.
Armed with fluorescent markers that bind to active virus particles, the scientists could differentiate between neurons with active viral infection and neurons in which the virus was present, but was not actively spreading, explains Prof. Ronald Goldstein, member of BIU’s Life Sciences faculty and mentor of doctoral student Amos Marcus, who actually built the model.
Then they set out to purposely awake the virus in order to figure out exactly how that happens.
Emotional shock factors into the equation because it can cause our immune response to flag. Numerous studies have shown correlations: even merely taking an exam can suppress cellular immunity and chronic stressors depress both cellular and humoral immune systems.
The Bar Ilan crew couldn't make their neurons take exams or crash a car, but after a lot of experimentation, they did manage to wake up the virus inside (which they saw using the fluorescent markers).
"For VZV, this is the first time that such re-activation has been achieved in a laboratory environment,” Goldstein said.
One eureka moment was realizing the implication of the fact that both chicken pox blisters and those charming herpes blisters are on our outer skin, not our innards. The team therefore cooled their neurons to 34 degrees centigrade – three degrees below body temperature, and found that the pace of VZV reactivation got a lot faster.
Now let us hope new medications that frustrate our VZV in the bud can be developed. No animals were hurt in the making of this model, by the way.
The BIU team collaborated on the model with Prof. Paul Kinchington of the departments of Ophthalmology and of Microbiology and Molecular Genetics at the University of Pittsburgh, who has made key discoveries about proteins involved in VZV activity.
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