Herpes simplex virus (HSV), including type 1 (HSV-1) and type 2 (HSV-2), is highly prevalent and establishes a lifelong presence in the body. While the virus is known for causing periodic outbreaks, such as cold sores or genital lesions, it spends considerable time in a “dormant” state within the nervous system. A common concern is whether the virus can be passed to a partner when no symptoms are present. The answer is yes, and understanding the biology of the virus during this quiet period is important for managing transmission risk.
The Biology of Herpes Latency
The term “dormant” refers to viral latency, a key survival strategy for the herpes simplex virus. After infecting the skin or mucosal tissue, the virus travels along nerve pathways to sensory nerve cell clusters called ganglia. HSV-1 typically settles in the trigeminal ganglia near the skull, while HSV-2 often resides in the sacral ganglia at the base of the spine.
Once inside the neuron, the viral DNA integrates and largely shuts down the genes responsible for producing new virus particles. The virus hides from the immune system in this protected location, establishing a stable, persistent infection. While latent, the virus is not actively reproducing or causing an outbreak, but it remains a permanent reservoir. Periodically, various triggers can cause the virus to reactivate and travel back down the nerve to the skin surface, initiating viral activity.
Asymptomatic Viral Shedding
The direct answer to transmission during dormancy is asymptomatic viral shedding. This is the process where the virus reactivates minimally and travels to the skin or mucosal surface without causing visible sores or symptoms. The virus is present on the skin surface in low concentrations and can be transmitted through direct skin-to-skin contact.
Asymptomatic shedding is unpredictable and occurs intermittently, but it is the primary mechanism by which the virus is spread between partners. Studies indicate that a significant majority, up to 70%, of new genital herpes infections are transmitted when the source partner had no symptoms. For those with genital HSV-2, shedding occurs on approximately 10.6% of days per year in the absence of treatment.
Modulating Factors of Transmission Risk
Several biological factors influence the likelihood of asymptomatic viral shedding and the risk of transmission. The type of herpes simplex virus is a major differentiator in shedding frequency. Genital infections caused by HSV-2 are associated with a much higher rate of asymptomatic shedding compared to genital infections caused by HSV-1, which sheds on only about 1.3% of days per year.
The duration of the infection is another factor, as shedding frequency tends to decrease over time. Individuals who recently acquired the virus are more likely to shed frequently than those infected for many years. A person’s immune status also plays a role, with factors like emotional stress, concurrent illnesses, or immunosuppression acting as triggers for viral reactivation and increased shedding. Transmission is also biologically easier from a male to a female partner than the reverse.
Strategies for Reducing Asymptomatic Spread
Fortunately, highly effective strategies exist to mitigate the risk of spreading the virus during asymptomatic shedding. The most impactful intervention is daily suppressive therapy using antiviral medications like valacyclovir, acyclovir, or famciclovir. Taking a daily antiviral pill significantly reduces the frequency of both symptomatic outbreaks and asymptomatic viral shedding.
This suppressive regimen has been shown to reduce the rate of asymptomatic shedding by approximately 70% to 75%. When used consistently, daily suppressive therapy reduces the risk of transmitting genital HSV-2 to a susceptible partner by nearly 50%. Consistent use of barrier protection, such as condoms, also provides moderate protection against transmission. Open and honest communication with partners about one’s status remains a fundamental part of managing and minimizing risk.