Cold sores come from a virus that hides for life in a facial nerve
Once the herpes simplex virus gets in, it never leaves. After the first infection it retreats up a nerve to a cluster of cells beside the brain called the trigeminal ganglion and lies dormant, sometimes for months. In roughly a third of people it periodically wakes, travels back down the nerve and raises blisters on the lip.
The usual culprit is herpes simplex virus type 1, occasionally type 2, spread mostly by ordinary non-sexual contact. Exposure is extremely common: by age 20 around 80 per cent of people carry antibodies to the virus. Yet only about 2.5 in every 1000 people have an outbreak in a given year, and most infections produce no symptoms at all. Among those who get recurrences, flare-ups usually happen fewer than three times a year and tend to become rarer with age.
The folk names cold sore and fever blister reflect a real pattern, because fevers such as those accompanying a cold often trigger an attack. Sunlight, psychological stress and menstrual periods can set one off too. The medical term, herpes labialis, uses the Latin word for lip.
A recurrence follows a fairly predictable timetable. It starts with tingling and redness, then within a couple of days come tiny, hard, tender bumps and fluid-filled blisters, usually on the lip or its border but sometimes on the nose, chin or cheeks. Around day four they burst and merge into a single weeping ulcer, the most painful and contagious stage, since the fluid teems with virus. From about day five a golden crust forms; it is made from blood serum rich in antibodies, not from live virus. Over the second week new skin grows beneath a series of ever-smaller scabs while the virus withdraws into hiding, and a red patch may linger even after they fall away.
A first infection can look quite different, inflaming the gums and cheek lining within 5 to 10 days, and in teenagers it often shows up as a severe sore throat.
Source: Cold sore
