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Anyone who’s ever suffered a cold sore knows the intermittent agony of coexisting with the herpes simplex virus type 1, or HSV-1. As many as 6 in 10 people in the U.S. harbor the virus without symptoms, but an unlucky few endure unpredictable outbreaks in which a painful blister erupts, festers, and fades away, only to reemerge months or even years later.

In rare cases, infections can lead to serious conditions like blindness and encephalitis. Now, a multidisciplinary research team at �ٺ���Ƶ Health has discovered how the virus evades the immune system—a critical discovery that paves the way for novel therapies to treat and potentially eradicate HSV-1 and other herpes viruses.

Infectious viruses engage in a kind of molecular arms race with the immune system, as both invader and host compete to take the lead. If all goes well for the host, the immune system eventually overwhelms the virus and eliminates it. But some viruses, including herpes simplex viruses, have evolved a clever tactic to linger on: a hibernation state known as viral latency, which allows viruses to lie dormant in a host’s cells, out of sight of the immune system. “Viruses can lurk in a human forever without causing disease,” explains , professor of microbiology. “But they can also reactivate, cause symptoms, and spread to a new host.”

Dr. Mohr, along with other colleagues at NYU School of Medicine, recently published a paper in the journal Cell Reports describing intriguing new details about how HSV-1 reawakens and, in the process, evades the host’s immune system to reproduce.

As with all herpes virus infections, HSV-1 infections are cureless and lifelong. The virus burrows into the nervous system, nesting deep inside the base of the brain, in an area of nerve cells called the trigeminal ganglion. “These nerve cells represent a stable place in which a latent virus can remain unperturbed for years,” explains study coauthor , professor of cell biology, and neuroscience and physiology. But how viruses emerge from this sanctuary has been poorly understood, in part because it’s difficult to study ganglion cells in isolation. “The ganglion is like a miniature organ,” explains Dr. Mohr. “It contains many different types of cells, including immune cells.”

The researchers’ solution was an innovative culturing technique “made of nothing but neurons,” says Dr. Mohr. “It allows us to study the molecular signaling and circuitry in depth, without interference from other cells.” With a clear window onto the infected cells, the researchers made a startling discovery: when jostled awake by stress, HSV-1 bursts into action, releasing a flood of proteins that jams the host’s immune reaction to interferon signals from infected cells, effectively disarming the cells’ alarm system. “This happens in the very first instant that HSV-1 reactivates,” explains , an associate professor of microbiology and another of the paper’s coauthors.

The findings may have implications for understanding other, more harmful pathogens that also exhibit latency, like varicella zoster, a herpes virus that causes chicken pox and shingles, and even tuberculosis and HIV. “This work is very exciting,” says Elisabeth J. Cohen, MD, professor of ophthalmology who is leading a federally funded, multicenter study of varicella zoster infections of the eye, a potentially serious complication that can result in blindness and chronic pain. “When these viruses come out of latency, they can cause many problems,” adds Dr. Cohen, who was not involved in the herpes simplex research. “If you can understand the process by which that happens, you might be able to find new ways to prevent them from causing harm.”

Currently, infections with both HSV-1 and varicella zoster are treated with antiviral drugs. These medications block the virus from replicating, which can eliminate symptoms of infections, but they are not a cure.

“The holy grail of this research is to one day eradicate latency either by getting the virus out or sealing it up permanently,” says Dr. Mohr. “Understanding all the interactions between viruses and hosts could yield findings that result in better treatments for a number of viral diseases. There are many implications, and we’ve only scratched the surface.