In the first century CE, Roman Emperor Tiberius made an unprecedented decision— banning kissing at all public events.
This move was aimed at thwarting a puzzling outbreak, which many historians believe was an epidemic of oral herpes.
Fast forward to today and more than half the population is infected with herpes simplex virus, though as many as 90 of those infected don't actually know they have it.
The term herpes virus refers to a whole family of viruses, but what we typically call the condition of herpes is caused by two viruses in particular herpes simplex 1 and 2, or HSV-1 and HSV-2.
While similar, they tend to infect different parts of the body.
HSV-1 is typically associated with oral herpes, which causes cold sores on the mouth.
Genital herpes can be caused by either virus, though it's more often caused by HSV-2.
Other body parts, such as fingers and eyes, can also be infected by either virus.
Regardless of location or type, HSV enters the body through microscopic breaks in the skin or mucus membranes, like the mouth and genitals.
Once inside, viral proteins hijack the cellular machinery to replicate and spread.
For many people, this initial infection won't result in any symptoms.
But for others the virus causes enough damage that fluid-filled blisters develop and rupture, causing painful lesions.
With more severe initial infections, the virus can enter the bloodstream and lead to fevers, muscle aches and headaches.
This viral onslaught alerts the immune system, which gets to work, attempting to eliminate the HSV virus, just as it would when faced with other common viral pathogens.
But what makes HSV particularly difficult to clear is that some virus hides itself away, evading detection by the immune system.
You see, in addition to penetrating skin and mucosal cells, HSV also infiltrates nearby nerve cells in the skin.
They then travel along the stretch of axons until they reach nerve clusters called ganglia.
HSV-1 thrives in the trigeminal ganglia located in the skull, and HSV-2 prefers the sacral ganglia near the base of the spinal cord.
Here the virus goes dormant, turning off its replication machinery, which helps it avoid attacks from the immune system.
It doesn't cause any damage or disease symptoms, but it doesn't disappear either.
While living in the ganglia.
The virus can reawaken periodically, often triggered by sickness or stress, though the cause isn't always clear.
No matter the reason, the virus travels back down along the nerve, which may cause itching or tingling, often the first symptom of recurrence.
Once back at the surface, the virus begins to replicate, potentially causing a new bout of symptoms.
The frequency of these recurrences can vary and happen as often as monthly or as infrequently as every few years.
And when the infection is active and shedding from the skin or mucosa, it's possible to spread to others via direct contact.
Yet since most infections are asymptomatic or only cause mild flare-ups, many people don't know they have HSV, and herpes is surprisingly difficult to diagnose.
Blood tests aren't normally recommended, as they're often inaccurate and can't reliably distinguish between a genital or oral HSV-1 infection.
If you do have symptoms, the best way to get a clear diagnosis is to see a health care provider when a lesion is present.
Aside from the pain caused by sores during a flare-up, for most people herpes doesn't lead to serious health problems.
And there are treatments to improve symptoms.
Antiviral medications work by mimicking a component of viral DNA and inhibiting viral replication.
These medications can also reduce the risk of transmission, in the case of HSV-2, by about 50%.
Over time.
Symptoms and shedding usually decline as the body produces immunity against the virus, though there is always some risk of flare-ups and transmission.
That's why for decades, scientists have searched for treatments that can prevent or cure herpes.
But the virus' unique ability to establish silent infections and evade the immune system has made progress difficult.
Still, there's hope.
Breakthroughs in emerging technologies like gene editing and novel vaccines show promise in the fight against this stealthy virus.
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