Once you catch infection, your immune system spares no effort to get rid of it. This protective mechanism works perfect for common cold and flu, but not for herpes infection.
According to statistic data, more than half Americans live with herpes simplex virus.
There are two types of this infection. Herpes type 1 affects mouth, causing cold sores and blisters, while herpes type 2 influences on genital area, making it itchy, swollen and painful.
Unlike flu virus, herpes runs quickly into the latent (or dormant) condition, when enters human's body. This helps virus hide from your immune system and exist inside the body for a long time.
When some external factors, like stress, hormonal changes or even exposure to sunlight, trigger awakening, replication and spreading of herpes virus, you may notice characteristic sores, blisters and redness near the mouth or genitals.
Numerous studies tried to find the way, herpes enters the latent mode. But it was really hard to put virus into the “sleep” form because investigators used isolated neurons in their experiments.
Now, specialists from the Princeton University developed new technique, which mimics natural three-chamber structure of the nerves.
It was found that after infection invades peripheral tissues, virus gets into the axons (connective pathways between the peripheral part and nerve cells) and then spread into the distant cell nucleus. There viral genome becomes dormant and may stay “asleep” during many days and even years.
Medical professionals say that your immune system normally kills infected cells, in order to eliminate virus away from the body. But in the case of herpes, it means that nerve cells should be destroyed. Unfortunately, human's neurons are irreplaceable. That's why keeping virus in “sleeping” pattern might be the optimal way to protect your nervous system.
During the study, experts tried to wake infection up in two ways: delivering stress signals, which trigger virus reproduction, and using so-called viral tegument proteins.
It was supposed that viral load (amount of virus cells, present in the body) is the main factor, which determines immune response. But it was found that viral tegument proteins by themselves act as the key triggers, activating herpes infection.
To date, researchers want to find out, whether this wake up-mechanism will work in the human organism, just as it works in the lab tests.
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