Etiology of Oral Herpes
Oral herpes is caused by herpes simplex virus type 1 (HSV-1), which is acquired through direct contact with infected lesions or body fluids, typically saliva. 1
Viral Agent and Transmission
HSV-1 is the primary causative agent of oral herpes (herpes labialis), though HSV-2 can also cause oral infections, particularly through oro-genital sexual practices 1
The virus is transmitted through direct contact with infected lesions or body fluids, most commonly saliva 2
HSV-1 is a nuclear replicating enveloped virus that establishes infection at mucocutaneous sites 2
Pathophysiology and Latency
After primary infection, HSV-1 establishes latent infection in the cervical ganglia (specifically the trigeminal ganglion neurons that innervate the oral mucosa) 1
During latency, the virus remains in a non-multiplying episomal form in the nuclei of neurons in the ganglia 1
The viral genome is maintained in a non-infectious state during latency but can reactivate in response to various triggers 3
Primary Infection Characteristics
Primary herpetic infection occurs when an HSV-seronegative person acquires HSV-1, typically during childhood 1
Primary infections are either asymptomatic or manifest as mucocutaneous vesicular eruptions after an incubation period of approximately 1 week 2
Children may develop severe oro-pharyngitis (herpetic gingivostomatitis) following primary exposure to HSV-1, affecting the tongue, lips, gingiva, buccal mucosa, and hard and soft palate 1, 2
The incubation period is typically 2 to 10 days (up to four weeks) 1
Recurrent Infection Mechanism
Recurrent herpetic infection results from reactivation of latent virus in the cervical ganglia 1
Common triggers for reactivation include:
Recurrences typically manifest as herpes labialis (cold sores or fever blisters) at mucocutaneous junctions, particularly the lips 2
Epidemiology
HSV-1 affects 20-40% of the adult population with recurrent cold sores 4, 5
Seroprevalence increases progressively from childhood and is inversely related to socioeconomic background 2
The infection represents a life-long condition with potential for periodic reactivation 1
Clinical Significance
Peak viral titers occur in the first 24 hours after lesion onset, with vesicles containing thousands of infectious viral particles 4, 6
In immunocompromised patients, recurrent infection can be more extensive, aggressive, and potentially involve the oral cavity or extend across the face 6
Most cases (80-90%) progress subclinically but may become symptomatic at any time 1