Herpes simplex virus infects skin or mucous membranes, causes painful sores or blisters, then hides inside nerve cells for life. Over 846 million people between 15 and 49 have a genital herpes infection worldwide, and billions more carry the oral form. The virus comes in two types: HSV-1, which typically causes cold sores around the mouth, and HSV-2, which usually causes genital herpes. Both types follow the same basic playbook once they enter your body.
How the Virus Gets Into Your Cells
Herpes is a contact virus. HSV-1 spreads mainly through saliva, sores, or skin contact in and around the mouth, though it can also reach the genitals through oral sex. HSV-2 spreads during sexual contact with genital or anal skin, sores, or fluids. HSV-2 infects women nearly twice as often as men because sexual transmission is more efficient from men to women.
Once the virus lands on skin or a mucous membrane, it latches onto the surface of a cell using proteins on its outer envelope. It then “surfs” along the cell surface until it reaches the main body of the cell, where it fuses its outer layer with the cell membrane and slips inside. From there, the viral DNA travels to the cell’s nucleus and hijacks the cell’s own machinery to make copies of itself. Those copies burst out to infect neighboring cells, which is what produces the visible sore.
What Happens During an Outbreak
The first outbreak is usually the worst. It typically shows up within two weeks of exposure and can include flu-like symptoms: fever, swollen glands, headaches, and body aches in the legs or buttocks. The hallmark signs are itching, tingling, or burning at the site of infection, followed a few days later by painful blisters or open sores.
Those blisters eventually crust over and heal, usually within two to four weeks for a first episode. Future outbreaks tend to be shorter, milder, and less frequent over time. Many people notice a tingling or burning sensation in the area a day or two before sores appear, a warning phase called the prodrome. Over years, outbreaks often become rare or stop entirely, though the virus never leaves the body.
How the Virus Hides for Life
This is what makes herpes permanent. After the initial infection in your skin, the virus travels along nerve fibers into clusters of nerve cells called ganglia. HSV-1 typically settles in the trigeminal ganglion near the base of the skull. HSV-2 usually takes up residence in the sacral ganglia near the base of the spine. Once inside a neuron, the virus goes dormant. It stops making most of its proteins and produces only a single molecule called the latency-associated transcript, which keeps the nerve cell alive and the virus hidden.
Your immune system does detect that something is wrong. Specialized immune cells cluster around the infected neurons and monitor them, catching and suppressing small flickers of viral activity. But the virus has evolved countermeasures. It dials its protein production down so low that immune cells can barely detect it, and infected neurons display surface markers that actually prevent immune cells from destroying them. The result is a stalemate: your immune system keeps the virus in check but can never fully clear it.
Periodically, the virus reactivates. It travels back down the nerve fiber to the skin surface, where it can cause a new outbreak or simply shed invisibly. Triggers for reactivation vary from person to person but commonly include stress, illness, fatigue, sun exposure, and hormonal changes.
Viral Shedding Without Symptoms
One of the most important things herpes does is spread even when you feel perfectly fine. This is called asymptomatic shedding, and it’s responsible for a large share of new infections. During the first six months after infection, the virus can be present on the skin surface 20% to 40% of days with no visible sores. Over time, shedding becomes less frequent, dropping to roughly 5% to 20% of days. But it never stops entirely, which is why herpes spreads so efficiently through populations. At least 42 million people acquire a new genital herpes infection every year, roughly one person every second.
Effects Beyond Sores
For most people, herpes means occasional or infrequent outbreaks of blisters that heal on their own. But the virus can cause serious complications in certain situations.
When herpes reaches the eye, it causes a condition called herpes keratitis, an infection of the cornea that is a major cause of blindness worldwide. Mild cases heal without lasting damage, but repeated or severe infections can scar the cornea permanently. In very rare cases, the virus can travel to the brain and cause herpes encephalitis, a life-threatening inflammation that requires emergency treatment.
Newborns face the highest risk. If a pregnant person contracts genital herpes for the first time during the third trimester, particularly in the last six weeks, the baby can be exposed to the virus during vaginal delivery. Neonatal herpes can affect the skin, eyes, mouth, or central nervous system and can be fatal. The risk drops significantly if the mother’s infection is older, because her immune system has had time to produce antibodies that cross the placenta and offer the baby some protection.
How Antiviral Treatment Works
There is no cure for herpes, but antiviral medications can shorten outbreaks, reduce their severity, and lower the chance of passing the virus to others. The most common antiviral works by mimicking one of the building blocks of DNA. Only cells actively infected with herpes convert the drug into its active form, which is why it targets the virus without harming healthy cells. Once activated, the drug inserts itself into the growing chain of viral DNA and stops it cold, because the drug molecule is missing a chemical group needed to attach the next piece. The virus can’t finish copying itself, and the outbreak stalls.
People with frequent outbreaks can take a daily antiviral to suppress reactivation. This approach cuts outbreak frequency significantly and reduces asymptomatic shedding, lowering transmission risk to sexual partners. For people with infrequent outbreaks, taking the medication at the first sign of tingling can shorten an episode by a day or two.
HSV-1 vs. HSV-2 in Practice
Both types cause the same kind of sores and follow the same pattern of latency and reactivation, but they behave differently depending on location. HSV-1 reactivates frequently in the mouth but tends to cause fewer and milder recurrences when it infects the genitals. HSV-2 does the opposite: it’s well-adapted to the genital area and causes more frequent outbreaks there, but rarely recurs when it infects the mouth. You can carry both types simultaneously. An estimated 50 million people worldwide have both HSV-1 and HSV-2 genital infections at the same time.
More than 200 million people experienced at least one symptomatic genital herpes episode in 2020, but a large number of people with herpes never have noticeable symptoms at all. They carry and shed the virus without knowing it, which is a major reason the infection is so widespread.