The Herpes Simplex Virus (HSV), which includes HSV-1 (oral herpes) and HSV-2 (genital herpes), is an extremely common infection globally. After initial exposure, the virus is never fully eliminated from the body, instead entering a quiet phase known as latency or dormancy. This state allows the virus to persist indefinitely without causing active symptoms, yet maintaining the potential to reactivate.
Understanding How Herpes Enters Latency
When the herpes virus first infects the body, it initially replicates in the epithelial cells at the site of entry, such as the mouth or genitals. From this peripheral site, the virus quickly accesses the ends of sensory nerves that innervate the infected tissue. It then travels backward along the nerve fibers, a process called retrograde axonal transport, toward the nerve cell body.
The virus’s destination is the clusters of nerve cells known as ganglia, such as the trigeminal ganglia for HSV-1 or the sacral ganglia for HSV-2. Once the viral genome reaches the nucleus of the neuron, it circularizes and settles into a non-replicating state. This is the establishment of latency, a state of truce with the host immune system.
During latency, the virus shuts down the expression of almost all its genes that would lead to active replication and the production of new virus particles. This tight repression of lytic genes is maintained by the cell’s own machinery and is characterized by the expression of a non-coding RNA called the Latency-Associated Transcript (LAT). By minimizing its activity and hiding within the protected environment of the nerve cell, the virus avoids being detected and destroyed by the body’s immune defenses.
Common Triggers for Reactivation
The dormant virus can be “woken up” and switch back into an active replication phase, leading to an outbreak, by a variety of internal and external factors. These triggers essentially disrupt the delicate balance that keeps the virus suppressed in the nerve ganglia. Physical stress is a common culprit, which includes having a fever, contracting another illness, or undergoing surgery.
Emotional stress is also frequently cited as a factor, as chronic long-term stress can weaken the immune system’s ability to keep the virus in check. Exposure to strong ultraviolet (UV) light, such as from sun exposure, can trigger oral herpes outbreaks. Physical trauma or irritation to the area where the virus is dormant, like friction from sexual intercourse or dental procedures, can also cause the virus to reactivate.
Hormonal changes, such as those that occur during the menstrual cycle, can influence the frequency of outbreaks. Any condition that causes immune suppression, like certain medications or illnesses such as HIV, can significantly increase the likelihood of the virus becoming active. Often, however, no identifiable trigger can be pinpointed, as the virus can spontaneously reactivate.
How Long the Virus Can Remain Latent
Once an individual is infected, the Herpes Simplex Virus remains latent in the body for the remainder of that person’s life. The virus is never eliminated, and the potential for it to reactivate is permanent. The term “dormant” refers to the period when the virus is present in the nerve cells but is not actively replicating or causing visible symptoms.
It is possible for this dormant phase to last for decades, with some individuals never experiencing a noticeable outbreak after their initial infection. A significant number of people who carry the virus may go their entire lives without developing any symptoms. The initial infection may have been so mild it was mistaken for something else, or it may have been completely asymptomatic.
The experience varies widely among individuals; some people may have only one or two outbreaks in their lifetime, while others may experience recurrences several times a year. Outbreaks tend to become less frequent and less severe over time as the body’s immune system learns to better control the virus.
Even when the virus is truly latent and not causing sores, there can be periods of asymptomatic viral shedding. This means the virus reactivates briefly and travels to the skin or mucous membranes without producing a visible lesion, allowing for potential transmission. HSV-2 tends to reactivate and shed more frequently than HSV-1.