Humans typically acquire HSV-1 as a primary infection of the mucosa of the lips or eye. During the initial acute infection, the virus replicates locally in the mucosal epithelium and gains access to the sensory nerve termini that underlie the skin’s surface. The virus then travels to the nerve cell bodies in the trigeminal ganglia where the virus will replicate in some cells and become latent in others. During the latent infection, the virus remains dormant in the trigeminal ganglion. During this period no infectious virus is detected, and viral gene expression is suppressed, except for the latency-associated transcript (LAT). Periodically, stress causes the virus to reactivate. During reactivation viral lytic gene transcription and DNA replication initiates in some neurons, and virions are transported back down the axons to the primary site of infection. This results in infectious virus at the site of initial infection, and in some instances, clinical lesions such as cold sores will result.