Herpes Simplex Virus Type 2 (HSV-2), the cause of most genital herpes cases, can remain dormant for years, often for an entire lifetime. HSV-2 is a chronic, lifelong infection that establishes viral latency shortly after initial exposure. During latency, the virus is present but mostly inactive, resulting in long periods, even decades, without noticeable physical symptoms. This ability to alternate between active and inactive states explains why many individuals are unaware they are infected and how the virus persists and is transmitted.
How HSV-2 Establishes Viral Latency
The long period of dormancy is rooted in the virus’s unique interaction with the human nervous system. Following initial infection at the skin or mucosal surface, virus particles travel along sensory nerve fibers to a cluster of nerve cells called a ganglion. For genital herpes, HSV-2 targets the lumbosacral dorsal root ganglia, located at the base of the spine. Once inside the nerve cell nucleus, the viral DNA circularizes and enters the latent phase, which differs fundamentally from the active phase.
During latency, the virus does not actively replicate or produce new infectious particles. Instead, it maintains a quiet presence by expressing only a few specific genetic sequences, such as the latency-associated transcript (LAT). LAT expression helps the virus survive and prevents the infected nerve cell from dying, preserving a viral reservoir. This latent state is difficult for the immune system to detect and for antiviral medications to target, which is why there is no cure. The virus remains indefinitely in the nerve cell nuclei as an episome, ensuring lifelong persistence.
Understanding Reactivation Triggers
Although the virus can remain dormant for years, the latent virus can be prompted to leave the nerve cell and travel back to the skin surface in a process called reactivation. Reactivation is often triggered by various forms of stress that temporarily compromise the body’s stability.
Common triggers include periods of physical stress, such as fever, illness, or surgery. Emotional stress is also a factor, as chronic anxiety can weaken the immune system’s protective function. Hormonal changes, such as those during the menstrual cycle, can correlate with increased reactivation likelihood. Additionally, direct physical irritation to nerve endings, like excessive friction from sexual intercourse, can stimulate the dormant virus.
Factors causing immune suppression, such as chemotherapy or advanced HIV infection, also increase susceptibility to reactivation. When the virus reactivates, it begins to replicate, potentially causing a symptomatic outbreak of blisters or sores. It can also lead to periods of viral shedding without visible symptoms. The frequency and severity of reactivations typically decrease over time as the immune system better manages the infection.
The Reality of Asymptomatic Transmission
The long-term dormancy of HSV-2 poses a significant challenge because it allows the virus to spread even when the infected person has no symptoms. This phenomenon is called asymptomatic viral shedding, referring to brief, intermittent periods when the virus travels to the skin surface and is released from nerve endings.
Shedding occurs when the virus is active enough to be contagious but not active enough to cause a visible lesion or outbreak. Studies show viral shedding occurs on approximately 20% of days in individuals with established HSV-2 infection. Most sexual transmissions of HSV-2—estimated to be around 80%—happen during these asymptomatic periods. This explains why most people contract genital herpes from a partner who was unaware of their infection or had no visible symptoms.
Because the infection can lay dormant for years, a type-specific blood test is the most effective way to determine a person’s status in the absence of lesions. Daily suppressive antiviral therapy can significantly reduce the frequency of asymptomatic shedding and lower the risk of transmission to a partner. However, a low risk of transmission still exists, making barrier methods a continuing consideration for risk reduction.