Cold sores, also known as recurrent herpes labialis, are caused by the herpes simplex virus type 1 (HSV-1). HSV-1 is a lifelong virus because of its ability to establish a site of latent infection and remain dormant in the sensory ganglia until it is reactivated by triggers such as illness, stress, sun exposure, or trauma to the lip. This entry reviews the prevalence of cold sores, along with the pathogenesis, triggers, and stages of a cold sore.
Initial infection with HSV-1 usually occurs during childhood, and patients remain asymptomatic until an outbreak occurs. It is known that by the fifth decade of life approximately 80% of adults have antibodies to HSV-1, indicating previous infection. Another 20% to 40% (50 million) people suffer from recurrent outbreaks of cold sores in the same location on the perioral (mouth) area. Recurrent cold sore outbreaks typically occur 2 to 3 times per year. For most people the frequency of recurrence declines after the age of 35.
The HSV-1 is a member of the Herpesviridae family. The transmission of HSV-1 occurs through direct contact with the oral secretions, mucosal surfaces, or lesions of an infected person who is actively shedding the virus. For instance, the HSV-1 is spread through kissing or sharing utensils with a person who is infected with the virus. Even if a person does not have an apparent lesion at the time of transmission, viral shedding could be happening, and this is another source of transmission. The HSV is composed of 4 main components: (1) a core that contains viral DNA and protein surrounded by (2) a nucleocapsid, (3) the tegumet (a layer of proteins that surrounds the capsid), and (4) an outer lipid-containing envelope. Viral glycoproteins project from the envelope, bind, and penetrate the host cell. HSV then binds to the receptors on the host cell, and the envelope fuses with the plasma membrane of the host cell. Envelope fusion allows the HSV nucelocapsid to enter the host cell and release its viral DNA. Viral replication leads to cell death and fusion of cells, leading to formation of blisters and localized inflammation.
A unique characteristic of the HSV is its ability to remain dormant in the host. Postinfection, HSV establishes a chronic latency in the dorsal root ganglia of the trigeminal and facial nerves. Latency of the HSV is lifelong, and patients do not have any apparent signs or symptoms of a cold sore during the latent phase. The latent virus may be reactivated at any time. Once reactivated, the virus replicates in the ganglion and travels via sensory nerves to cause a recurrent outbreak. Recurrent cold sores typically occur at the site of primary infection. However, it is not unlikely that a cold sore could develop at another spot in the perioral area.
Reactivation of cold sores is often the result of common triggers such as stress, sun exposure, illness (cold, flu), fatigue/poor nutrition, menses, facial trauma, severe chapping of the lips, wind/cold weather, and immunosuppression. People who have the HSV-1 virus are well aware of the triggers that cause them to have an outbreak.
Once a patient is stricken with a cold sore, he or she goes through many stages prior to the complete healing of the cold sore. The life span of a cold sore is between 9 and 12 days. Day 1 is considered the “prodrome” stage. During the prodrome, the skin in the perioral area will be red, throbbing, tingling, or swollen. It is important to remember that the majority of cold sores usually occur on the border of the mouth. On days 2 and 3, fluid-filled blisters (vesicles) form on an erythematous base. The size of these blisters varies. On the fourth day, the vesicles rupture, causing the sore to weep fluid that is very contagious. This is considered the most painful stage. During days 5 to 8, a yellow-colored crust develops, and the patient experiences burning and tingling. This is the start of healing process for the cold sore. Anytime between days 9 and 12, the crust eventually falls off. The skin may still flake, and the area may be red. However, at this point the lesion is technically healed.
In conclusion, the goals of therapy for a patient who experiences cold sore outbreaks are to improve one's quality of life, reduce the duration of symptoms, shorten the healing time, prevent transmission, and prevent further outbreaks. There are several over-the-counter and prescription drugs approved for such therapy.
(1) The lesion associated with labial herpes (see HERPES SIMPLEX ). (2) The recurrent thin-walled vesicular mucocutaneous lesion associated...
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[NOTE: cold sore] (kōld sōr) Colloq. usage for labial lesion due to herpes simplex virus infection. altmed dent derm id ...