New herpes study reveals ‘important’ information

Scientists have discovered how the dreaded herpes virus enters our cells.

Herpes simplex virus type 1, the main cause of oral herpes, enters nerve cells by taking over cellular transport processes, according to a new article in the journal Proceedings of the National Academy of Sciences.

This discovery could help researchers develop new, more effective treatments against this sneaky and surprisingly common virus.

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Herpes simplex type 1 (HSV-1) is primarily responsible for oral herpes. About 67 percent of people under the age of 50 worldwide, or 3.7 billion, are infected with the virus, which can cause outbreaks of cold sores on and around the mouth. Herpes simplex type 2 (HSV-2) primarily causes genital herpes, with 13% of people aged 15 to 49 worldwide, or approximately 490 million people, infected with this virus. Both types of viruses can cause symptoms in both the mouth and genital areas, but the majority of oral herpes is caused by HSV-1 and the genitals by HSV-2.

These viral infections are spread by skin-to-skin contact, usually by kissing for HSV-1 and by sexual contact for HSV-2, infecting nerve cells. Many people never experience symptoms of herpes simplex infection, but those who do experience painful blisters in the infected areas, which may return after long periods of dormancy. Triggers for a recurrent flare-up may include sun exposure, stress, surgery, illness, or fever. There is no cure yet for infections with these viruses because they reside in the nervous system.

According to the new paper, herpes could enter our nerve cells using structures called microtubules and using special protein motors called dynein and kinesin to move.

Dynein is a tiny protein found in cells that acts like a small motor and helps move objects inside the cell. This can include transporting food particles, waste and other materials where they need to go. Dynein works by running along tracks inside the cell called microtubules, heading primarily toward the center of the cell. Kinesin is another type of motor protein, like dynein, but it usually moves in the opposite direction. Kinesin “walks” along the same microtubules as dynein, but generally heads toward the outer parts of the cell.

“We are developing vaccines against these viruses and these vaccines have been designed specifically not to get into your nervous system,” said study author Gregory Smith, professor of microbiology and immunology at Northwestern University, in a press release. “We knew how to mutate them so that they didn’t reach the nervous system. But we didn’t completely understand, from a mechanistic point of view, why our mutations were so effective.”

Northwestern University researchers describe how they attached special fluorescent markers to the virus to observe how it moved within an infected cell. They found that a protein in the virus called pUL37 hijacks and deactivates the cell’s kinesin to speed its journey to the nerve cell’s nucleus.

“Our results demonstrate how alphaherpesviruses, such as HSV-1, have evolved to become highly efficient at invading the nervous system,” study co-author DongHo Kim, a Ph.D. student in the Smith lab, said in the release. “The virus achieves this by spatially and temporally regulating the kinesin motor protein to allow smooth delivery of virus particles to the nucleus. Failure to regulate the kinesin motor will cause it to engage in a tug-of-war with the opposing dynein motor , and the virus fails to move in one direction or another.

Researchers hope to use these findings to potentially create new treatments for herpes infections.

“I think our model adds a significant step in understanding the process of neuroinvasion by HSV-1, and I am personally excited to see how we can use this machinery for potential therapies,” Kim said.

“With this new understanding, we can now delve deeper into this choreographed process that transmits viral genetic material from the outside world to our neurons,” Smith agreed.

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