Glycolic acid, a widely used alpha hydroxy acid (AHA), is a popular ingredient in cosmetic and dermatological products valued for its exfoliating properties. It is important to clarify that glycolic acid does not cause cold sores, as these lesions are the result of an infection by the Herpes Simplex Virus type 1 (HSV-1). However, for individuals who already carry the dormant HSV-1, the chemical exfoliation process can act as a significant trigger that leads to a viral reactivation and the subsequent outbreak of a cold sore.
Understanding Glycolic Acid and Chemical Exfoliation
Glycolic acid is characterized by its small molecular structure, which allows it to penetrate the skin’s outermost layer, the stratum corneum, effectively. Its primary function is to facilitate chemical exfoliation by dissolving the bonds between dead skin cells, known as corneocytes. The acid weakens the intercellular cement that holds these cells together. This controlled dissolution of cellular bonds results in the uniform shedding of the skin’s surface layer.
The process reveals the newer, underlying skin cells and stimulates the turnover of keratinocytes. This action is intentional and beneficial for skin appearance, but it represents a form of controlled chemical irritation or trauma to the skin surface.
The depth and intensity of this chemical trauma depend heavily on the concentration and pH of the glycolic acid product used. Mild, over-the-counter formulations typically cause very superficial exfoliation, while high-concentration products used in professional chemical peels can create a more substantial inflammatory response. This temporary disruption of the skin barrier, even when controlled, is the mechanism that links the use of glycolic acid to the potential for viral reactivation.
The Nature of Cold Sores and Viral Latency
Cold sores are a recurring manifestation of the Herpes Simplex Virus type 1 (HSV-1), which establishes a lifelong presence after the initial infection. Once the primary infection resolves, the virus retreats into a dormant state known as latency. For oral herpes, the virus takes refuge primarily in the sensory nerve cells of the trigeminal ganglion near the ear. In this latent state, the viral genetic material remains inactive, producing little active virus.
The virus can remain dormant for years without ever causing symptoms. However, the latent virus is highly sensitive to various environmental and physical stressors that can signal it to reactivate. Common, non-chemical triggers for reactivation include exposure to ultraviolet (UV) radiation from the sun, acute physical stress like fever or illness, hormonal fluctuations, and physical trauma to the face or lips. When one of these stressors occurs, the virus travels back down the nerve pathway to the skin surface, resulting in the characteristic blistering outbreak.
How Exfoliation Acts as a Reactivation Trigger
The controlled chemical irritation inflicted by glycolic acid is recognized as a localized physical trauma, serving as a potent trigger for dormant HSV-1. When a glycolic acid solution is applied, especially in the high concentrations typical of professional peels, it initiates an inflammatory and immune response. This response is perceived as a stress signal by the latent virus in the trigeminal ganglion, signaling it to exit its dormant state.
The reactivated virus then travels along the nerve axon back to the skin cells surrounding the application area, most commonly around the mouth or lips. This viral migration and subsequent replication in the epidermal cells result in the visible cold sore outbreak.
The risk of reactivation is directly proportional to the intensity of the trauma; a high-concentration glycolic acid peel presents a greater risk than a low-concentration, at-home product. Any procedure that causes skin injury, including chemical peels, microdermabrasion, or laser resurfacing, can initiate this process in HSV-1 carriers.
Strategies for Safe Glycolic Acid Use
Individuals with a history of cold sores who plan to use glycolic acid, especially in a professional peel setting, should take proactive steps to mitigate the risk of an outbreak. The most effective preventative measure is the use of prophylactic antiviral medication. Consulting a physician for a prescription antiviral drug, such as acyclovir or valacyclovir, is strongly advised before undergoing a procedure.
Antiviral therapy should begin one to two days before the peel and continue for several days afterward, as directed by a healthcare provider. This medication works to suppress the viral replication process, preventing the virus from establishing an active infection at the skin’s surface. For at-home use, starting with a low concentration of glycolic acid (5% or less) can help assess the skin’s tolerance and reaction.
It is also important to avoid applying glycolic acid products directly to the area immediately surrounding the lips, where HSV-1 outbreaks typically occur. If any tingling, itching, or burning sensation—early signs of an impending outbreak—are felt before or after a treatment, the application should be stopped immediately.
Even individuals without a known history of cold sores can experience an outbreak following a stressor like a chemical peel. Discussing your history with a skincare professional before treatment is advised.