Since HSV infections are not reportable diseases, good statistics on the occurrence of infections in the United States are not available. The NHANES II study conducted from 1970 to 1984 (16
) and the NHANES III study conducted between 1985 and 1994 (10
) demonstrated that a significant number of adults in the United States are infected with HSV-2, the STD of herpesviruses. A 30% increase in HSV-2 seroprevalence has been seen in the last decade alone (10
). This study confirms the earlier observation that HSV-2, in general, is more prevalent in women than in men (10
). This conclusion is supported by the observation that over two-thirds of all positive cultures in this institution were obtained from women, and over three-fourths of all HSV-2 cultured from clinical specimens originated from women. HSV-2 was seen primarily in genital cultures, with only a small proportion seen in nongenital sites. The year 1998 stands out as an exception to this rule, with 26.2% of patients having HSV-2 in nongenital locations. Although only 11 patients with nongenital HSV-2 were identified during this year, this represented over one-third of the cases identified over the 6-year period. The relative decrease in the total number of positive cultures made this increase in nongenital HSV-2 cases seem even more inflated when percentages were determined. Overall, patients presenting with HSV-2 in nongenital sites represented less than 10% of cases for the remaining years, a proportion similar to that seen in other studies (8
While HSV-2 has traditionally been viewed as the marker for sexually transmitted HSV, this ignores the role that HSV-1 also serves in causing genital herpes. It has generally been accepted that approximately 10 to 15% of newly acquired genital herpes is actually caused by HSV-1 (1
). Regional variation in the percent of genital herpes caused by HSV-1 has been noted, however. Several locations in Britain have reported that up to 50% of cases of newly acquired herpes genitalis are caused by HSV-1 (5
). The current data suggest that the proportion of HSV-1 in genital specimens also has increased dramatically in Central Kentucky, with the 1999 data demonstrating that over 43% of female genital isolates and over 30% of male genital isolates are HSV-1. Since HSV-2 is known to produce more genital reactivations than HSV-1 (22
), it would be expected that HSV-2 would have more opportunities to be cultured. This would potentially skew detection of genital herpes in favor of HSV-2 isolates. Despite this fact, HSV-1 genital herpes has shown a significant increase in genital sites in this study.
The explanation for this increased proportion of genital HSV-1 is not clear, but might be explained by several potential mechanisms. First, this trend may be due to the decreasing rate of HSV-1 immunity in young adults. Several studies support this theory. A cross-sectional study of 1,057 college students found that the 18- to 19-year-old population had only 32.7% seropositivity compared to those over 20 who demonstrated 43.5% HSV-1 seropositivity (12
). Similarly, a cohort of 14- to 15-year-olds who were monitored for 15 years initially had a 25% seropositivity for HSV-1, but had a 59% seropositivity 15 years later (6
). A 1975 university-based study of HSV respiratory disease indicated that only 30% of incoming students initially had HSV-1 antibodies, but there was an approximate 10% annual rate of seroconversion noted in this population (13
). Of note, in a recent study looking at 124 healthy 17- to 24-year-olds in Central Kentucky, only 35.1% of the 17- to 19-year-olds had antibodies to HSV-1. In the 20- to 24-year-old group, the seroprevalence had risen to 46.8% indicating that there was a gradual seroconversion seen in this population (unpublished data).
Linked to this apparent expanded population at risk for delayed infection also is probably a change in the sexual practices leading to an increase in oral-genital contact. Demographic analysis of individuals with primary genital HSV-1 has indicated that 50 to 100% of these patients had experienced oral-genital contact within weeks of their outbreak (8
). These studies suggest that the practice of oral-genital sex is ubiquitous among those individuals acquiring herpes genitalis. A survey of sexual practices administered to individuals presenting to a Denver clinic for HIV testing likewise indicated that oral sex was quite commonly practiced in this patient population, with 88.7% acknowledging having had oral sex as a risk factor for acquiring an STD (26
). While one might not be able to generalize these observations to the general population, it seems likely that individuals presenting for evaluation of genital ulcer disease will have engaged in oral sex a significant proportion of the time.
Several issues may be influencing this apparent increase in the practice of oral-genital sex. In a recent survey of college students, 59% indicated that they felt that oral-genital contact did not constitute actually “having had sex” for the sake of preserving virginity (30
). A potential benefit of limiting sexual activity to oral-genital intercourse could therefore include maintaining ones “virginal state.” In a 1983 study of female university students, 35% of those who considered themselves “virgins” had engaged in oral-genital acts. This compared to 97% of “non-virgins.” suggesting that other factors also motivate oral-genital behaviors (15
). Oral-genital intercourse appears to be a socially acceptable current practice, with over 80% of men and women surveyed in 1999 acknowledging having had some “oral-genital experience.”
Other influences on having oral-genital sex might include the perceived notion that oral sex is “safe sex.” Although oral sex does preclude conception, unprotected receptive oral genital intercourse is not safe from an infectious disease standpoint. Transmissions of Neisseria gonorrhoeae
), human immunodeficiency virus (32
), human papilloma virus, hepatitis C, and molluscum contagiosum (9
) through unprotected oral-genital contact have all been documented. Transmission of HSV from an individual with active herpes pharyngitis or herpes labialis may likewise occur during oral-genital contact (9
). The inoculation of HSV in high titer onto uninfected genital mucosa has been demonstrated to cause lesions and lead to reactivation disease in these new locations (24
). Since individuals with herpes infections may shed infective virus without any evidence of active lesions (20
), there would be no disease-free periods during which oral contact could be absolutely risk-free with regard to viral transmission.
Nonsexual transmission of HSV-1 also may occur by autotransmission. This could include transmission of viral particles from oral lesions through the gut to the perineum or by the direct inoculation of virus to the genitals on fingers or fomites. The parasthesias associated with herpes labialis often lead patients to repeatedly touch the infected lesion. Virus carried on the fingers could then be transferred directly to the perineum during the placement of tampons or indirectly transferred on toilet paper if adequate hand washing prior to toileting is not performed. In vivo studies of autoinoculation from one site to another with the patient's own strain of HSV has been demonstrated to cause new foci of disease and reactivation (24
). The spread of genital HSV onto the patient's fingers or eyes or onto mucocutaneous sites adjacent to primary genital regions late in the disease course suggests that autoinoculation is a common occurrence (7
). It is unclear why this rate of transmission would be showing such a dramatic increase with time, unless it was concluded that personal hygiene and hand washing practices have changed significantly.