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   [ Back to EurekAlert! ] Public release date: 27-Mar-2013   
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   Contact: marla Paul   
   marla-paul@northwestern.edu   
   312-503-8928   
   Northwestern University    
   How herpesvirus invades nervous system   
   Viral protein hijacks cellular machinery and grabs the wheel   
   (Chicago) - Northwestern Medicine scientists have identified a component of   
   the herpesvirus that "hijacks" machinery inside human cells, allowing the   
   virus to rapidly and successfully invade the nervous system upon initial   
   exposure.   
   Led by Gregory Smith, associate professor in immunology and microbiology at   
   Northwestern University Feinberg School of Medicine, researchers found that   
   viral protein 1-2, or VP1/2, allows the herpesvirus to interact with cellular   
   motors, known as dynein.    
   Once the protein has overtaken this motor, the virus can speed along   
   intercellular highways, or microtubules, to move unobstructed from the tips of   
   nerves in skin to the nuclei of neurons within the nervous system.   
   This is the first time researchers have shown a viral protein directly   
   engaging and subverting the cellular motor; most other viruses passively hitch   
   a ride into the nervous system.   
   "This protein not only grabs the wheel, it steps on the gas," says Smith.   
   "Overtaking the cellular motor to invade the nervous system is a complicated   
   accomplishment that most viruses are incapable of achieving. Yet the   
   herpesvirus uses one protein, no    
   others required, to transport its genetic information over long distances   
   without stopping."   
   Herpesvirus is widespread in humans and affects more than 90 percent of adults   
   in the United States. It is associated with several types of recurring   
   diseases, including cold sores, genital herpes, chicken pox, and shingles. The   
   virus can live dormant in    
   humans for a lifetime, and most infected people do not know they are disease   
   carriers. The virus can occasionally turn deadly, resulting in encephalitis in   
   some.   
   Until now, scientists knew that herpesviruses travel quickly to reach neurons   
   located deep inside the body, but the mechanism by which they advance remained   
   a mystery.   
   Smith's team conducted a variety of experiments with VP1/2 to demonstrate its   
   important role in transporting the virus, including artificial activation and   
   genetic mutation of the protein. The team studied the herpesvirus in animals,   
   and also in human    
   and animal cells in culture under high-resolution microscopy. In one   
   experiment, scientists mutated the virus with a slower form of the protein   
   dyed red, and raced it against a healthy virus dyed green. They observed that   
   the healthy virus outran the    
   mutated version down nerves to the neuron body to insert DNA and establish   
   infection.   
   "Remarkably, this viral protein can be artificially activated, and in these   
   conditions it zips around within cells in the absence of any virus. It is   
   striking to watch," Smith says.   
   He says that understanding how the viruses move within people, especially from   
   the skin to the nervous system, can help better prevent the virus from   
   spreading.   
   Additionally, Smith says, "By learning how the virus infects our nervous   
   system, we can mimic this process to treat unrelated neurologic diseases. Even   
   now, laboratories are working on how to use herpesviruses to deliver genes   
   into the nervous system and    
   kill cancer cells."   
   Smith's team will next work to better understand how the protein functions. He   
   notes that many researchers use viruses to learn how neurons are connected to   
   the brain.   
   "Some of our mutants will advance brain mapping studies by resolving these   
   connections more clearly than was previously possible," he says.   
   ###   
   This work was funded by grants R01 AI056346, R01 EY017809, T32AI07476 from the   
   National Institute of Allergy and Infectious Diseases of the National   
   Institutes of Health.   
   It was published in the journal Cell Host & Microbe and is available online at   
   http://www.sciencedirect.com/science/article/pii/S1931312813000401.   
      
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