Cold sores are caused by herpes simplex virus type 1, commonly called HSV-1. An estimated 3.8 billion people under age 50 carry this virus, roughly 64% of the global population. Most picked it up during childhood through casual contact like a kiss from a family member, and many never develop visible sores at all.
HSV-1 vs. HSV-2
There are two types of herpes simplex virus. HSV-1 is the primary cause of oral cold sores, while HSV-2 is traditionally associated with genital herpes. That said, the distinction isn’t absolute. A six-year study of nongenital herpes cultures found that about 9.4% of cases were caused by HSV-2 rather than HSV-1. So while HSV-2 can occasionally show up on the lips or face, it’s responsible for fewer than 1 in 10 oral herpes cases.
How the Virus Gets Into Your Cells
HSV-1 spreads through direct contact with infected skin or saliva. Once the virus reaches skin cells, it latches onto receptors on the cell surface using proteins embedded in its outer envelope. After attaching, it “surfs” along the cell surface until it reaches the main body of the cell, then fuses its outer membrane with the cell’s membrane and releases its genetic material inside.
That viral DNA travels into the cell’s nucleus, where it hijacks the cell’s machinery to make copies of itself. In regular skin cells, this replication happens rapidly, producing the inflammation and blistering you see during an outbreak. In nerve cells, however, the virus takes a different path: it goes quiet.
Why Cold Sores Keep Coming Back
After your first infection, HSV-1 travels along nerve fibers and settles into a cluster of nerve cells near the base of the skull called the trigeminal ganglion. There, the virus enters a dormant state called latency. During latency, the virus barely produces any proteins, making it essentially invisible to your immune system. Your body does station immune cells in the ganglion to keep watch. These specialized T cells appear to suppress the virus through noncytolytic pathways, meaning they control it without killing the neurons it hides in.
The virus also protects itself during this dormant phase. It produces a molecule called the latency-associated transcript, which shields the infected neurons from self-destructing. This is why HSV-1 is a lifelong infection. The virus isn’t actively replicating, but it’s not gone either. It’s waiting.
What Triggers an Outbreak
A variety of stressors can wake the virus from dormancy: psychological stress, fever, UV light exposure (sunburn on the lips is a classic trigger), illness, or physical trauma to the area. These triggers seem unrelated on the surface, but they converge on a shared biological pathway. Stress causes your body to release cortisol through the hormonal stress response. Cortisol activates a receptor inside cells called the glucocorticoid receptor, which enters the cell nucleus and can switch on viral gene promoters, essentially flipping the virus back into active mode.
UV light activates that same receptor through a different mechanism that doesn’t even require cortisol. Heat stress raises cortisol levels directly. The result is the same across triggers: the virus begins replicating in the nerve cell, travels back down the nerve fiber to the skin surface, and produces a new outbreak.
The Five Stages of a Cold Sore
Once reactivated, a cold sore typically progresses through five distinct stages over 7 to 14 days:
- Tingling: A prickling or burning sensation around the lips, often the first warning sign before anything is visible. This prodrome stage is when antiviral treatment is most effective.
- Blistering: Within a day or two, small fluid-filled blisters appear on or near the lip.
- Weeping: The blisters rupture within a few days, leaving shallow, red open sores. This is the most contagious stage.
- Crusting: The open sore dries out and forms a yellowish or brown crust.
- Healing: The scab gradually flakes away as new skin forms underneath.
Spreading Without Visible Sores
One of the trickiest aspects of HSV-1 is that it can be contagious even when no sore is present. This is called asymptomatic shedding, when the virus is active on the skin surface without producing visible symptoms. Research tracking people with herpes found shedding on about 12% of days at two months after infection, dropping to 7% of days by 11 months. For most of those shedding episodes, participants had no symptoms at all. Over time, shedding rates continue to decline, falling to around 1.3% of days two years after infection in one group studied.
This means kissing, sharing utensils, or sharing lip products can transmit the virus even when someone looks and feels perfectly fine. It also explains why HSV-1 is so widespread globally.
Treatment and Timing
Antiviral medications can shorten outbreaks and reduce their severity, but timing matters. Treatment is most effective when started within one day of the sore appearing, or ideally during the tingling prodrome stage before blisters form. Prescription antivirals work by blocking the virus’s ability to replicate, which limits how much damage it can do to surrounding tissue.
For people who get frequent outbreaks (six or more per year), daily suppressive antiviral therapy can reduce the number of flare-ups and lower the chance of transmitting the virus to others. Over-the-counter creams containing docosanol can also modestly shorten healing time if applied early, though prescription antivirals are more effective.
When the Virus Spreads Beyond the Lips
Cold sores are usually a nuisance rather than a danger, but HSV-1 can occasionally affect other parts of the body. The most concerning complication is herpes keratitis, an infection of the cornea. This typically happens when the virus reactivates and travels to the eye rather than the lip, or when someone touches a cold sore and then rubs their eye. Herpes keratitis is a leading infectious cause of corneal blindness, and recurrences can cause progressive scarring. Symptoms include eye redness, pain, tearing, light sensitivity, and blurred vision.
HSV-1 can also infect the fingers (called herpetic whitlow), spread to larger areas of skin in people with eczema, or in rare cases cause encephalitis, a serious brain infection. These complications are uncommon but worth knowing about, particularly the importance of not touching an active cold sore and then touching your eyes or broken skin elsewhere on your body.