Shingles is a painful, blistering rash caused by the reactivation of the virus that causes chickenpox. After the initial infection clears, the virus remains in a quiet, dormant state within the body. A shingles flare-up occurs when the body’s control over this sleeping virus weakens, allowing it to multiply and travel. Understanding the specific factors that disrupt this balance between the virus and the immune system is important for recognizing the risks.
How the Virus Reactivates
The virus establishes a permanent, inactive residence within the body’s nerve tissue after the initial chickenpox infection resolves. It typically settles in clusters of nerve cells near the spinal cord, known as the dorsal root ganglia. In this latent phase, the virus remains quiet, kept in check by the immune system.
A shingles flare-up begins when the dormant virus reactivates and replicates within the nerve cells. The virus then travels along the nerve fiber (axon), moving away from the spinal cord. This migration continues until the virus reaches the skin surface, causing the characteristic painful, unilateral rash in the area supplied by that specific nerve.
Chronic Immune Vulnerability
The primary, long-term cause of a shingles flare is a sustained decline in the body’s specific immune surveillance against the virus. The immune system uses specialized white blood cells, called T-cells, to constantly monitor the nerve ganglia and suppress viral activity. When the effectiveness of these T-cells drops below a certain threshold, the virus is given the opportunity to awaken.
Age is the greatest risk factor because T-cell immunity naturally wanes over time. The incidence of shingles increases dramatically after age 50, and the risk continues to escalate, particularly in individuals over 80. This age-related weakening of the immune system is the most common chronic vulnerability allowing the virus to reactivate.
A number of underlying chronic illnesses also compromise immune function, creating vulnerability at any age. Conditions such as HIV/AIDS, certain blood cancers, and autoimmune disorders directly impair the T-cell response needed to keep the virus dormant. These diseases create an environment where the immune system is chronically suppressed, greatly increasing the likelihood of a viral flare-up.
Acute Lifestyle and Emotional Triggers
Temporary, short-term factors can acutely suppress the immune system, allowing the virus to reactivate. Psychological stress is a documented trigger, primarily because chronic emotional strain elevates the production of cortisol. Cortisol is a stress hormone known to suppress the function of infection-fighting white blood cells, including T-cells.
Sustained high cortisol levels reduce the body’s ability to maintain its defense against dormant viruses. This compromise in immune vigilance can provide the necessary window for the virus to begin its journey down the nerve. Severe fatigue and a lack of restorative sleep also negatively impact T-cell function, further weakening the immune barrier.
Acute physical events can also act as localized or systemic triggers for a flare. A severe, short-term illness, such as the flu, can temporarily divert immune resources away from surveillance of the nerve ganglia. Localized physical trauma to an area of the body can sometimes precede a shingles rash appearing in that exact location.
Medications and Medical Intervention
Certain medical treatments and medications are designed to suppress the immune system and are significant, deliberate triggers for viral reactivation. Immunosuppressive drugs are commonly prescribed to prevent organ transplant rejection or to manage severe autoimmune conditions. These medications directly target and reduce the activity of T-cells, which increases the risk of a shingles flare-up.
High-dose corticosteroids, a class of powerful anti-inflammatory drugs, are strongly associated with increased risk. Doses equivalent to more than 20 milligrams of prednisone per day are considered high-risk, as they significantly dampen the immune response. Other agents, including certain chemotherapy drugs and biologics, also suppress T-cell function, making the body more susceptible to the virus escaping latency.
Radiation therapy for cancer treatment can also severely compromise a patient’s immune status, particularly when the treatment field includes areas near the spine where the virus resides. The general immune suppression caused by these interventions provides the opportunity for the virus to multiply unchecked.