Key Differences Between HSV-1 and HSV-2
HSV-1 and HSV-2 are distinct viral serotypes that differ primarily in their anatomical site preferences, recurrence patterns, and epidemiological characteristics, though the traditional distinction of "above the neck" versus "below the waist" is increasingly blurred due to oro-genital sexual practices. 1, 2
Anatomical Distribution and Transmission
HSV-1 traditionally manifests above the neck (orolabial region, lips, mouth, face) and is typically acquired through non-sexual contact, often during childhood via saliva or direct contact with infected lesions 1, 3
HSV-2 typically affects areas below the waist (genital mucosa, penile and labial skin, perigenital region) and is almost always sexually transmitted 1
This anatomical distinction is not absolute: 20-25% of genital herpes cases are now caused by HSV-1 due to oro-genital sexual practices, while HSV-2 can cause 4-7% of orofacial infections 4, 5
Epidemiology and Prevalence
HSV-1 has substantially higher prevalence: approximately 57.7% of the US population aged 14-49 years are seropositive for HSV-1 6
HSV-2 prevalence is lower: approximately 17.0% of the US population aged 14-49 years are seropositive for HSV-2 6
HSV-1 seroprevalence increases progressively from childhood and is inversely related to socioeconomic status 3
Recurrence Patterns - A Critical Clinical Difference
HSV-2 recurs much more frequently in the genital area than HSV-1, with significantly higher monthly recurrence frequency 2
This difference in recurrence rates is crucial for patient counseling and has important implications for transmission risk and quality of life 1, 2
Clinical Manifestations
Primary HSV-1 infection typically presents as gingivostomatitis with fever, irritability, tender submandibular lymphadenopathy, and painful oral/perioral ulcers 2, 3
Primary HSV-2 infection typically presents as genital herpes with local symptoms including pain, pruritus, dysuria, vaginal/urethral discharge, and inguinal lymphadenopathy 2
Both infections share similar lesion evolution: sensory prodrome followed by progression from papule to vesicle, ulcer, and crust stages 2
Most genital herpes cases (80-90%) are asymptomatic regardless of viral type, though they may become symptomatic at any time 2
Latency Sites
HSV-1 establishes latency in the trigeminal ganglia (innervating the upper half of the body) 2, 5
HSV-2 establishes latency in the sacral ganglia (innervating the lower half of the body) 2, 5
Clinical Implications and Complications
HSV-2 is a significant risk factor for HIV acquisition and can increase HIV RNA levels in coinfected patients 2
There is considerable stigma associated with HSV-2 infection because it is almost always associated with genital disease, whereas HSV-1 is associated with both oro-pharyngeal and genital disease 1
Both infections are lifelong, with the virus remaining in a non-multiplying episomal form in neural ganglia during latency periods 2
Diagnostic Considerations
Type-specific testing is essential because it helps predict recurrence patterns and guides patient counseling 1, 2
Viral culture or validated nucleic acid amplification tests (NAATs) are recommended for symptomatic patients 1
Type-specific serology should differentiate between HSV-1 and HSV-2 using glycoprotein G-based assays, though HSV-2 serologic tests have specificity issues, particularly with index values <3.0 1
HSV-2 serologic testing should not be repeated until 12 weeks after exposure due to the window period for antibody development 1
Common Pitfall
The most important clinical pitfall is assuming genital herpes is always HSV-2 or that oral herpes is always HSV-1. With 20-25% of genital herpes now caused by HSV-1, type-specific testing is critical because HSV-1 genital infections have substantially lower recurrence rates than HSV-2, which dramatically affects prognosis, counseling, and patient quality of life 1, 4.