• We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Logo of straninfSexually Transmitted InfectionsVisit this articleSubmit a manuscriptReceive email alertsContact usBMJ
Sex Transm Infect. Jun 2006; 82(3): 189–190.
PMCID: PMC2564733

Genital HSV‐1 infections

Short abstract

Importantly, individuals with genital HSV‐1 are still at risk of HSV‐2 acquisition

Keywords: herpes simplex virus, seroprevalence

In the past decade, investigations have amply documented the increase in the frequency of genital herpes simplex virus type 1 (HSV‐1) compared with genital HSV‐2 infection. This trend has been seen both in Europe and in the United States, and it is comprehensively documented in New South Wales, Australia, on p 255 of this issue of STI.1 The issues raised by this observation have implications for understanding changes in HSV seroprevalence and sexual behaviour over time, and for patient management and counselling.

What accounts for the rise in the frequency of genital HSV‐1? First of all, it needs to be acknowledged that genital HSV‐1 infection has been common for a long time. For example, a Japanese study of women, published in 1976, documented 43% of genital herpes as caused by HSV‐1.2 In 1977, a university health clinic study showed that 37% of women with clinical diagnosis of genital herpes had HSV‐1 isolated.3 Among people with newly acquired genital herpes in Seattle in the mid to late 1980s, 32% had genital HSV‐1 infection.4 Still, several well done studies have shown that the relative proportion of genital HSV‐1 isolates has increased even more strikingly in the past two decades.5,6,7 Two potential explanations that have been put forth include a decrease in HSV‐1 acquisition among children, leaving them susceptible to HSV‐1 in adolescence, and increase in oral‐genital contact, or initiation of oral sex instead of genital‐genital sex, among adolescents. Population based studies, although few have looked at secular trends in HSV‐1 infection, do not suggest a prominent decrease in HSV‐1 seroprevalence.8

Is oral sex more prevalent now than it was about 30 years ago? It seems unlikely that this practice has been invented by current youth, as occasionally portrayed by the news media, since ancient texts, including the Kama Sutra written between the 1st and 6th century ad, describe it. However, the concern about pregnancy among adolescents and about HIV among men who have sex with men may have tipped the balance in favour of this behaviour. In a peculiar way, abstinence proponents may have helped, as adolescents often does not regard oral sex as sex.9 The delay in vaginal intercourse among teenagers observed in the recent surveys suggests that oral sex has replaced vaginal intercourse among the younger teens. Finally, data from several centres have shown that women, rather than heterosexual men, are at high risk for genital HSV‐1.10,11,12 A small proportion of these women may have sex with women, a potential risk factor for genital HSV‐1, presumably because of the frequent practice of oral sex.13 Among heterosexual women, the increase is more difficult to explain as sexual behaviour surveys suggest that fellatio rather than cunnilingus is more likely to be practised.14,15 Most likely, these observations confirm women's inherent susceptibility to HSV infections compared with men, as the mucosal lining of the female external genitalia is likely to be more vulnerable than the thin but keratinised skin of male genitalia.

For appropriate clinical management and complete patient counselling, the type of virus needs to be identified

What do these changes imply for clinicians? In my view, the increase in genital HSV‐1 as a cause of genital herpes clearly shows the need for laboratory confirmation of the clinical diagnosis of genital herpes, and the need to identify the type of the virus. The signs and symptoms of the first episode or a recurrence are identical for both viral types. Genital HSV‐1, which almost always causes a true primary infection, is likely to be more severe during the initial episode. However, genital HSV‐1 causes fewer recurrences (few or none after the first year of infection) and is shed asymptomatically infrequently.16,17 These are critical counselling points to provide to affected patients. Importantly, individuals with genital HSV‐1 are still at risk of HSV‐2 acquisition, and it is not known whether previous genital HSV‐1 infection modifies the risk of HSV‐2 acquisition more substantially than previous oral HSV‐1 infection.18 Thus for appropriate clinical management and complete patient counselling, the type of virus needs to be identified. In a patient with a first episode of lesions, this is best done using viral culture or type specific polymerase chain reaction.

The risk of genital HSV‐1 infection has further muddled the issue of HSV serological testing that has been long in coming to assist in genital herpes diagnosis. For those who doubt the clinical utility of these assays, it is useful to remember that the clinical diagnosis of genital HSV‐2 infection is, at best, 39% sensitive and has a 20% false positive rate.19 Thus instead of comparing the “almost perfect” record of HIV antibody tests with HSV antibody tests, the added value of serological testing is clear when one recalls the limited accuracy of clinical diagnosis. The development of accurate serological assays has been hindered by extensive cross reactivity between antibodies to HSV‐1 and HSV‐2, and concerns remain about specificity and sensitivity of commercial serological tests that use only one or two antigens. However, aside from technical issues that may limit test performance, clinicians may struggle with the interpretation of the test.20,21,22 The message to the patient is clear when he or she presents with recurrent genital lesions and the test indicates presence of HSV‐2 antibody. But what do we tell a patient who tests positive for HSV‐1 only and has no history of oral and genital lesions? In my clinic, such patients are informed that we cannot tell where they have the infection. Among those with prevalent HSV‐1, most are likely to have acquired the infection in childhood. However, adults with incident HSV‐1 are equally likely to be infected in the mouth or the genital area, or perhaps, both. Since these people are asymptomatic, disease management is not of concern. However, susceptibility to HSV‐2, but probably not HSV‐1, still remains and potential risk of transmission provides information to patients.

Counselling a person with genital HSV‐1 about the risk of transmission presents an interesting predicament. While the propensity for both clinical and subclinical reactivation is dramatically lower for genital HSV‐1 than for genital HSV‐2, the neonatal data suggest that when reactivation recurs among HSV‐1 infected women during delivery, the virus is more likely to be transmitted with an estimated relative risk of ~60.23 Thus the infectivity, once present, appears greater for HSV‐1 than for HSV‐2. We do not know whether the increased risk of transmission also applies to sexual transmission. However, among 48 source partners of people with documented newly acquired genital HSV‐1, HSV‐1 was isolated from the genital area in seven and from the oral area in three (unpublished data). This suggests that genital to genital HSV‐1 transmission is potentially not uncommon. Many people do not think that current or potential partners need to be told about oral HSV‐1 infection, although this may change as more people are aware of their status. Avoiding mucosal contact with a clinically apparent cold sore, as well as protecting newborns from such contact, seems prudent, and patients should receive such education. Condom use is unlikely to have an impact on genital HSV‐1 acquired from oral sex, since most people do not use a barrier for such contact, and there is a paucity of studies of antiviral therapy for oral HSV‐1 infection. We can hope that the increase in genital HSV‐1 will spur research for an HSV vaccine that protects against acquisition of HSV‐1 and HSV‐2.

Footnotes

Supported by NIH Grant AI‐30731.

Conflict of interest: none.

References

1. Haddow L J, Dave B, Mindel A. et al Increase in rates of herpes simplex virus type 1 as a cause of anogenital herpes in western Sydney, Australia, between 1979 and 2003. Sex Transm Infect 2006. 82255–259.259 [PMC free article] [PubMed]
2. Kawana T, Kawaguchi T, Sakamoto S. Clinical and virological studies on genital herpes. Lancet 1976. 2964 [PubMed]
3. Kalinyak J, Fleagle G, Docherty J. Incidence and distribution of herpes simplex virus types 1 and 2 from genital lesions in college women. J Med Virol 1977. 1175–181.181 [PubMed]
4. Wald A, Benedetti J, Davis G. et al A randomized, double‐blind, comparative trial comparing high and standard dose oral acyclovir for first‐episode genital herpes infections. Antimicrob Agents Chemother 1994. 38174–176.176 [PMC free article] [PubMed]
5. Vyse A J, Gay N J, Slomka M J. et al The burden of infection with HSV‐1 and HSV‐2 in England and Wales: implications for the changing epidemiology of genital herpes. Sex Transm Infect 2000. 76183–187.187 [PMC free article] [PubMed]
6. Roberts C M, Pfister J R, Spear S J. Increasing proportion of herpes simplex virus type 1 as a cause of genital herpes infection in college students. Sex Transm Dis 2003. 30797–800.800 [PubMed]
7. Ribes J A, Steele A D, Seabolt J P. et al 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. 393321–3325.3325 [PMC free article] [PubMed]
8. Schillinger J A, Xu F, Sternberg M R. et al National seroprevalence and trends in herpes simplex virus type 1 in the United States, 1976–1994. Sex Transm Dis 2004. 31753–760.760 [PubMed]
9. Halpern‐Felsher B L, Cornell J L, Kropp R Y. et al Oral versus vaginal sex among adolescents: perceptions, attitudes, and behavior. Pediatrics 2005. 115845–851.851 [PubMed]
10. Janier M, Scieux C, Meouchi R. et al Virological, serological and epidemiological study of 255 consecutive cases of genital herpes in a sexually transmitted disease clinic of Paris (France): a prospective study. Int J STD AIDS 2006. 1744–49.49 [PubMed]
11. Coyle P V, O'Neill H J, Wyatt D E. et al Emergence of herpes simplex type 1 as the main cause of recurrent genital ulcerative disease in women in Northern Ireland. J Clin Virol 2003. 2722–29.29 [PubMed]
12. Lafferty W E, Downey L, Celum C. et al Herpes simplex virus type 1 as a cause of genital herpes: impact on surveillance and prevention. J Infect Dis 2000. 1811454–1457.1457 [PubMed]
13. Marrazzo J M, Stine K, Wald A. Prevalence and risk factors for infection with herpes simplex virus type‐1 and ‐2 among lesbians. Sex Transm Dis 2003. 30890–895.895 [PubMed]
14. DeBuono B A, Zinner S H, Daamen M. et al Sexual behavior of college women in 1975, 1986, and 1989. N Engl J Med 1990. 322821–825.825 [PubMed]
15. Gateley A, Gander R, Johnson P. et al Herpes simplex virus 2 meningoencephalitis resistant to acyclovir in a patient with AIDS. J Infect Dis 1990. 161711–715.715 [PubMed]
16. Engelberg R, Carrell D, Krantz E. et al Natural history of genital herpes simplex virus type 1 infection. Sex Transm Dis 2003. 30174–177.177 [PubMed]
17. Wald A, Zeh J, Selke S. et al Virologic characteristics of subclinical and symptomatic genital herpes infections. N Engl J Med 1995. 333770–775.775 [PubMed]
18. Sucato G, Wald A, Wakabayashi E. et al Evidence of latency and reactivation of both herpes simplex virus (HSV‐1) and HSV‐2 in the genital region. J Infect Dis 1998. 1771069–1072.1072 [PubMed]
19. Langenberg A, Corey L, Ashley R. et al A prospective study of new infections with herpes simplex virus type 1 and type 2. N Engl J Med 1999. 3411432–1438.1438 [PubMed]
20. Song B, Dwyer D E, Mindel A. HSV type specific serology in sexual health clinics: use, benefits, and who gets tested. Sex Transm Infect 2004. 80113–117.117 [PMC free article] [PubMed]
21. Krantz I, Lowhagen G B, Ahlberg B M. et al Ethics of screening for asymptomatic herpes virus type 2 infection. BMJ 2004. 329618–621.621 [PMC free article] [PubMed]
22. Page J, Taylor J, Tideman R L. et al Is HSV serology useful for the management of first episode genital herpes? Sex Transm Infect 2003. 79276–279.279 [PMC free article] [PubMed]
23. Brown Z A, Wald A, Morrow R A. et al Effect of serologic status and cesarean delivery on transmission rates of herpes simplex virus from mother to infant. JAMA 2003. 289203–9 See linked article on p255.9 See linked article on p255 [PubMed]

Articles from Sexually Transmitted Infections are provided here courtesy of BMJ Group
PubReader format: click here to try

Formats:

Related citations in PubMed

See reviews...See all...

Cited by other articles in PMC

See all...

Links

  • PubMed
    PubMed
    PubMed citations for these articles

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...