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With a kiss, herpes type 1 is permanently sealed.
HSV1 (herpes simplex virus type 1), which hibernates in the peripheral nervous system and cannot be eradicated, is carried by more than half of adults in the United States.
A new Northwestern Medicine study published in Nature has uncovered the virus’s devious strategy for infecting the nervous system, clearing the way for the development of long-awaited vaccines for both HSV1 and its close sibling HSV2.
Some HSV1 carriers will never get more than a cold sore as a result of the virus.
Others, on the other hand, may suffer from blindness or life-threatening encephalitis.
There is growing evidence that it plays a role in dementia.
HSV2, which is more commonly transmitted through sexual contact, can be passed from a mother to a newborn during the birthing process as neonatal herpes, which manifests as lesions on the infant’s body.
The majority of babies recover, but in the most severe cases, it can cause brain damage or spread throughout the body, resulting in death.
“A vaccine to prevent herpes from invading the nervous system is desperately needed,” said Gregory Smith, PhD, professor of Microbiology-Immunology.
A path to that has been discovered by Smith’s lab in a new study.
Herpes hijacks a protein from epithelial cells and turns it into a defector, allowing it to travel into the peripheral nervous system, according to the research.
The process has been dubbed “assimilation,” and it’s a breakthrough that could have far-reaching implications for a variety of viruses, including HIV and, according to Smith.
“The virus must inject its genetic code into the nucleus in order to begin producing more herpes viruses,” Smith explained.
“It turns the cell into a virus factory.”
The big question is, “How does it get to a neuron’s nucleus?”
Herpes uses protein engines called dynein and kinesin to move along microtubules in the cell, as do many viruses.
Herpes uses a kinesin engine that it brings from other cells to ferry it to the nucleus of the neuron, according to Smith’s team.
To serve the virus’s purpose, that kinesin protein becomes a defector.
“We can now think about how to take away that ability by learning how the virus achieves this incredible feat of getting into our nervous system,” Smith explained.
“You’d have a virus that couldn’t assimilate kinesin if you could stop it from doing so…
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