How the Immune System Fights to Keep Herpes at Bay

Herpes simplex virus (HSV) is extremely common, affecting nearly two-thirds of the world’s population, according to the World Health Organization.

Once inside the body, HSV establishes a latent infection that periodically awakens, causing painful blisters on the skin, typically around the nose and mouth. While a mere nuisance for most people, HSV can also lead to dangerous eye infections and brain inflammation in some people and cause life-threatening infections in newborns.

Researchers have long known that the virus and the host immune system are in a perpetual competition, but why does this battle reach a stasis in most people while causing serious infections in others?

More important, precisely how does the battle unfold at the level of cells and molecules? This question has continued to bedevil scientists and hamper the quest for treatments that prevent or cure infections.

A recent study by researchers at Harvard Medical School, conducted using lab-engineered cells and published in PNAS, unveils the precise maneuvers used by host and pathogen in the fight for dominance of the cell.

Furthermore, the research shows how the immune system keeps the virus at bay in a battle taking place at the control center of the cell — its nucleus.

Immune signaling proteins issue a call to arms

The research reveals a key role for a group of signaling proteins called interferons, which recruit other protective molecules and block the virus from establishing infection.

Once inside the host, HSV multiplies by making copies of itself inside the nuclei of cells, using the host’s genetic machinery. For that to happen, the virus must outcompete the host’s immune system. But many of the tactics the virus and the immune system use in this contest have remained a mystery, making it challenging to design medicines to help patients defeat the virus.

Interferons — named for their ability to interfere with pathogens’ attempts to infect cells — are signaling molecules released when the immune system detects the presence of microbes, such as viruses. The distress signals sent by interferons activate genes in that cell and other cells that produce proteins, which in turn block viruses from establishing infection in the first place.

Several different mechanisms that interferons use to thwart viruses within the cytoplasm, the gelatinous liquid that fills cells, are well known. But how interferons work against DNA viruses — those launching their attack within the cell nucleus — has remained elusive.

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