Northwestern Medicine scientists have identified a component¹ of the herpesvirus（疱疹病毒） that "hijacks²" machinery³ 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 cellular⁴ motors, known as dynein（动力蛋白）. 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 nuclei⁵ of neurons within the nervous system.

 

This is the first time researchers have shown a viral protein directly engaging and subverting⁶（颠覆，推翻） the cellular motor; most other viruses passively hitch⁷ 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 accomplishment⁸ that most viruses are incapable⁹ of achieving. Yet the herpesvirus uses one protein, no others required, to transport its genetic¹⁰ 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 recurring¹¹ diseases, including cold sores, genital herpes, chicken pox, and shingles¹². The virus can live dormant¹³ 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 mechanism¹⁴ 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 activation¹⁵ and genetic mutation¹⁶ 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 DNA¹⁷ and establish infection.

 

"Remarkably¹⁸, this viral protein can be artificially activated¹⁹, and in these conditions it zips around within cells in the absence of any virus. It is striking to watch," Smith says.

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