The current study has documented the predominant role of HSV-1 in the etiology of genital herpes in the Tel Aviv area during the 1993 to 2002 period. However, HSV-2 was rarely isolated from nongenital lesions. The only previous attempt to document the involvement of the two herpes types in genital lesions in Israel dates back to the 1970s. Out of 26 genital isolates, 24 (92%) were HSV-2 and 2 (8%) were HSV-1. 13 The high and rising proportion of HSV-1 genital lesions has been attributed to an increasing frequency of orogenital sex and perhaps to a declining incidence of HSV-1 infection in childhood. HSV-1 infection rates in children declined in the industrialized world during the 1950s and 1960s as a result of improved personal hygiene standards. Serologic surveys from the United Kingdom indicated that infection with HSV-1 was almost universal by the onset of adulthood during the 1940s, but had decreased to only 40% of adults by the 1960s. 14 In a survey of a small group of Israeli adolescents in 1998 to 1999, the prevalence of anti–HSV-1 antibodies was 45.7% in persons aged 11 to 14 years (35 tested), 53.8% in persons 15 to 17 years (39 tested), and 60.2% among 18- to 21-year-olds (171 tested). 15 Consequently, many Israeli youth enter the age of sexual activity with no HSV-1 antibodies, and constitute a reservoir of potential candidates for genital HSV-1 infection.
Orogenital sex has been gaining popularity, particularly among teenagers, because it cannot result in unwanted pregnancy and is believed not to transmit sexually transmitted diseases. 16 Lowhagen et al. 10 found a significant correlation between being infected with HSV-1 and having orogenital sex and a partner with a history of labial herpes. In another study, receptive oral sex in the preceding 2 months significantly increased the odds that the initial infections were HSV-1 rather than HSV-2. 17 However, if orogenital sex does play an important role in the sexual transmission of HSV, one should expect an increase in the isolation rate of HSV-2 from orolabial lesions. There is no clear evidence for such a trend. 18 However, in a recent report from Germany, 19 3 out of 18 persons with a positive HSV polymerase chain reaction result from a specimen taken at the orolabial site were found to shed HSV-2, suggesting that orolabial HSV-2 infection might be mostly asymptomatic.
Several studies have demonstrated an inverse relationship between the isolation rate of HSV-1 from genital lesions and the age of patients. 8–11 This trend was also observed in the current study, with the proportion of HSV-1 being significantly higher in persons aged 15 to 24 years than in those 45 years or older. Because recurrent clinical episodes and subclinical viral shedding are far less common in patients with genital HSV-1 than in those with HSV-2 infection, the proportion of HSV-1 isolates in primary lesions is significantly higher than that in recurrent episodes. 11,17 This issue was not examined in the current study because information regarding the stage of the sampled lesions was not available; nevertheless, it is likely that most of the isolates were derived from initial cases. Lafferty et al. 17 found that the proportion of HSV-1 among initial genital herpes infections was higher among men who have sex with men (46.9%) than among heterosexual men (14.6%). The retrospective design of our study did not allow us to obtain information regarding the sexual orientation and sexual practices of the patients who were tested. The overrepresentation of the female sex in the study population is most likely a result of the increased concern to diagnose the condition in women because of the potential obstetrical repercussions of an untreated infection.
The rising proportion of genital herpes due to HSV-1 may have some positive consequences. As mentioned previously, persons with genital HSV-1 infection have far fewer symptomatic recurrences and much less subclinical shedding than those with HSV-2 (approximately 0.02 and 0.33 per month, respectively), 20,21 so that genital HSV-1 infection is a lesser concern clinically and socially than HSV-2. Also, because of the same reasons, it was assumed that HSV-1 might be associated with fewer neonatal complications than HSV-2. However, a recent study 22 showed that the rate of transmission of HSV from mother to infant was higher when HSV-1 was isolated at delivery (31.1%) compared with HSV-2 (2.7%). Because of the higher sensitivity of HSV-1 to acyclovir and a lower rate of acute and long-term neurologic sequelae, the overall outcome of neonatal HSV-1 infections seems to be better than that of cases caused by HSV-2. 23
The concept that HSV-1 causes infection “above the waist” (orolabial herpes) and that HSV-2 causes infection “below the waist: (genital herpes) is no longer relevant. HSV-1 is, at present, the leading cause of genital herpes in many parts of the world. Consequently, seroprevalence studies that use HSV-2 type-specific assays significantly underestimate the incidence and prevalence of genital HSV infection
1. Cleator GM, Klapper PE. Herpes simplex. In: Zuckerman AJ, Banatvala JE, Pattison JR, eds. Principles and Practice of Clinical Virology, 4th ed. Chichester: Wiley 2000: 23–45.
2. Corey L, Adams HG, Brown ZA, Holmes KK. Genital herpes simplex virus infection: clinical manifestations, course and complications. Ann Intern Med 1983; 98: 958–972.
3. Ishiguro T, Ozaki Y, Matsunami M, Funakoshi S. Clinical and virological features of herpes genitalis in Japanese women. Acta Obstet Gynecol Scand 1982; 61: 173–176.
4. Wooley PD, Kudesia G. Incidence of herpes simplex virus type-1 and type-2 from patients with primary (first-attack) genital herpes in Sheffield. Int J STD AIDS 1990; 1: 184–186.
5. Ross JD, Smith IW, Elton RA. The epidemiology of herpes simplex type 1 and 2 infection of the genital tract in Edinburgh 1978–1991. Genitourin Med 1993; 69: 381–383.
6. Tayal Sc, Pattman RS. High prevalence of herpes simplex virus type 1 in female anogenital herpes simplex in New-castle upon Tyne 1982–93. Int J STD AIDS 1994; 5: 359–361.
7. Ribes JA, Steele AD, Seabolt JP, Baker DJ. Six-year study of the incidence of herpes in genital and nongenital cultures in a central Kentucky medical center patient population. J Clin Microbiol 2001; 39: 3321–3325.
8. Fotwafd KR. Recovery rates of herpes simplex type 1 (HSV-1) from patients with genital herpes in Nova Scotia. In: 42nd ICAAC Abstracts, American Society for Microbiology; September 27–30, 2002; San Diego, CA. Abstract L-771, p 354.
9. Roberts CM, Pfister JR. Increasing proportion of HSV-1 as a cause of genital herpes infection in college. Presented at the 2002 National STD Prevention Conference; March 4–7, 2002; San Diego, CA. Abstract LB1.
10. Lowhagen GB, Tunback P, Andersson K, Bergstrom T, Johannisson G. First episodes of genital herpes in a Swedish STD population: a study of epidemiology and transmission by the use of herpes simplex virus (HSV) typing and specific serology. Sex Transm Infect 2000; 76: 179–182.
11. Nilsen A, Myrmel H. Changing trends in genital herpes simplex virus infection in Bergen, Norway. Acta Obstet Gynecol Scand 2000; 79: 693–696.
12. Puthawathana P, Kanyok R, Horthongkham N, Roongpisuthipong A. Prevalence of herpes simplex virus infection in patients suspected of genital herpes, and virus typing by type specific fluorescent monoclonal antibodies. J Med Assoc Thai 1998; 81: 260–264.
13. Leventon-Kriss S, Rannon L, Smetana Z, Yoffe R. Genital herpes simplex infections in Israel: 1973 through 1980. Isr J Med Sci 1982; 18: 941–945.
14. Corey L, Spear PG. Infections with herpes simplex viruses. N Engl J Med 1986; 314: 686–691.
15. Isacsohn M, Smetana Z, Zakai Rones Z, et al. A sero-epidemiological study of herpes virus type 1 and 2 infection in Israel. J Clin Virol 2002; 24: 85–92.
16. Gagnon JH, Simon WS. The sexual scripting of oral genital contacts. Arch Sex Behav 1987; 16: 1–25.
17. Lafferty WE, Downey L, Celum C, Wald A. Herpes simplex virus type 1 as cause of genital herpes: impact on surveillance and prevention. J Infect Dis 2000; 181: 1454–1457.
18. Lippelt L, Braun RW, Kuhn JH. Genital herpes simplex virus type 1 infection: new field for an old acquaintance? Intervirology 2002; 45: 2–5.
19. Wolff MH, Schmitt J, Rahaus M, Dudda H, Hatzmann W. Clinical and subclinical reactivations of genital herpes virus. Intervirology 2002; 45: 20–23.
20. Lafferty WE, Coombs RW, Benedetti J, Critchlow C, Corey L. Recurrences after oral and genital herpes simplex virus infection. N Engl J Med 1987; 316: 1444–1449.
21. Wald A, Zeh J, Selke S, Ashley RL, Corey L. Virological characteristics of subclinical and symptomatic genital herpes infections. N Engl J Med 1995; 333: 770–775.
22. Brown ZA, Wald A, Ashley Morrow R, Selke S, Zeh J, Corey L. Effect of serologic status and cesarean delivery on transmission rates of herpes simplex virus from mother to infant. JAMA 2003; 289: 203–209.
23. Corey L, Whitley RJ, Stone EF, Mohan K. Difference between herpes simplex virus type 1 and type 2 neonatal encephalitis in neurological outcome. Lancet 1988; 1: 1–4.