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3-Recurrent Herpes labialis A prodrome of pain, burning & tingling Followed by the development of erythematous papules that rapidly develop into tiny, thin-walled, intraepidermal vesicles that become pustular and ulcerate In most patients, fewer than 2 recurrences each year, but some individuals have monthly recurrences Maximum viral shedding is in the first 24 hours of the acute illness but may last 5 days. 4-Primary genital herpes Primary genital herpes can be caused by both HSV-1 and HSV-2 Recurrences are more common with HSV-2 Asymptomatic in most patients Primary genital herpes is characterized by severe and prolonged systemic and local symptoms.
Clinical features in men Herpetic vesicles appear in the glans penis, the prepuce, the shaft of the penis, and sometimes on the scrotum, thighs, and buttocks In dry areas, the lesions progress to pustules and then crust Herpetic urethritis occurs in 30-40% of patients and is characterized by severe dysuria and mucoid discharge The perianal area and rectum can be involved in persons who engage in anal intercourse, resulting in herpetic proctitis. Clinical features in women Herpetic vesicles appear on the external genitalia, labia majora, labia minora, vaginal vestibule, and introitus In moist areas, the vesicles rupture, leaving exquisitely tender ulcers The vaginal mucosa is inflamed and edematous. In men and women, the ulcerative lesions persist from 4-15 days until crusting and reepithelialization occur The median duration of viral shedding is about 12 days. Subclinical genital herpes The majority of primary genital HSV infections are asymptomatic and 70%-80% of seropositive individuals have no history of symptomatic genital herpes Nevertheless, they experience periodic subclinical reactivation with virus shedding, thus making them a source of infection The rate of viral shedding may be 1-2%.
Tzanck smear is a time-honored procedure to assist in the diagnosis of cutaneous herpesvirusinfections Typically, an intact vesicle is used from which the vesicular fluid is aspirated After aspiration, the vesicle should be unroofed aseptically.Using a sterile instrument, the floor of the newly produced ulcer can then be scraped. Staining can be performed with a Papanicolaou stain,Gram or Giemsa A positive result is the finding of multinucleate giant cells. Umbilicated vesiculopustules that progress to punched-out erosions The eruption is most commonly disseminated in the areas of dermatitis, with a predilection for the head& trunk.
Pain may subside in 2-3 w in young patients but may last for 1 m in the elderly Pain lasting longer than 1-3 months is referred to as postherpetic neuralgia. Following resolution of the chickenpox, the virus lies dormant in the dorsal root ganglia until focal reactivation along a ganglion's distribution results in herpes zoster Although the exact precipitants that result in viral reactivation are not known certainly, decreased cellular immunity appears to increase the risk of reactivation. Genital herpes, most frequently caused by HSV-2, has become the leading cause of genital ulcer disease worldwide. Research findings have shown that being seropositive for HSV-2 can increase the risk of HIV acquisition among high-risk HIV-negative people exposed to HIV and, likewise, the infectiousness of individuals co-infected with HIV-1 and HSV-2 can increase during periods of HSV-2 reactivation.
WHO has recently issued new guidelines for the syndromic management of genital ulcer disease that include antiviral treatment for lesions consistent with genital herpes.
The United States Centers for Disease Control and Prevention issued updated Sexually Transmitted Diseases Treatment Guidelines in 2002 that recommended the use of type-specific serological tests for diagnosing HSV-2.
Recently launched proof-of-concept, HSV-2 intervention trials in several countries will help to determine the proportion of new HIV infections that could be prevented by suppression of HSV-2, and the findings from these studies will inform those involved in setting prevention and treatment priorities and strategies in developing countries.
A meta-analysis of studies on HSV-2 found that infection with HSV-2 doubled the risk of becoming infected with HIV through transmission during sexual activity (1). New prevention strategies are urgently needed to reduce the contribution of HSV-2 to HIV transmission, particularly in developing countries that have high prevalence of both HSV-2 and HIV.
HSV-2 causes ulcers and micro-ulcerations, which are often asymptomatic and thus unrecognized; these breaks in the mucosa and the skin in the genital area create portals for the entry of HIV. HSV-2 lesions contain substantial numbers of CD4+ lymphocytes, which are target cells for HIV. Laboratory studies have shown that these CD4+ lymphocytes are likely to facilitate the acquisition of HIV in HIV-negative, HSV-2-positive individuals when they are exposed to HIV. Episodes of reactivation of HSV-2 are associated with increased shedding of HIV from lesions and genital mucosa. Until very recently, most sexually transmitted disease (STD) interventions have focused on bacterial STIs, which are easier to diagnose and treat than genital herpes. As a result, little attention has been paid to the diagnosis of genital herpes and there has been a lack of prevention interventions; consequently, the epidemics of HSV-2 and HIV continue to fuel each other. In some parts of sub-Saharan Africa, where HIV is of great concern, the prevalence of HSV-2 among women is as high as 75% (2).
The options range from widespread screening for HSV-2 and suppressive antiviral therapy, to other strategies that may have benefits in reducing HSV-2 transmission as well as in HIV prevention.
Studies currently being conducted will provide more data on which policy-makers can base their decisions as to the most feasible and cost-effective approaches.
We (CC and AW) identified articles, reports and abstracts published during or after 2000.
Substantial biological data from in vivo and in vitro studies support the hypothesis that HSV-2 increases HIV infectiousness. The meta-analysis was based on the most rigorous studies that documented HSV-2 infection that had occurred prior to infection with HIV. They discovered a strong association between HSV-2 status and HIV seroconversion among the 70 male study subjects, and reported that 60 of these HIV seroconversions occurred in men with HSV-2 infection. The adjusted odds ratio for HIV incidence in HSV-2-positive men was higher for the male subjects who seroconverted to HSV-2 during the 2-year follow-up period than for those who were HSV-2-seropositive at baseline, suggesting that the severity and more frequent reactivation of new HSV-2 infections plays an important role in increasing the risk of HIV acquisition. Nine per cent of the young men and 34% of the young women in the study area were infected with HIV, and HSV-2 seroprevalence was almost twice as high (17% among men and 53% among women). HSV-2 seropositivity was strongly associated with HIV infection: men who were seropositive for HSV-2 were seven times more likely to be HIV-positive than men who were seronegative for HSV-2. Among the individuals infected with HIV, 91% of the women and 65% of the men were co-infected with HSV-2.

They reported that higher prevalences of HSV-2 in men and women, and of trichomoniasis in women and the lower prevalence of circumcision of males in the two cities that had a high prevalence of HIV played a greater role than sexual behaviour in explaining the differences in HIV prevalence between the four cities studied. Given the high HSV-2 seroprevalence in Kisumu and Ndola, Buvé and colleagues hypothesized that as the prevalence of HIV and HSV-2 increased in these cities, the two viruses fuelled transmission of one another by increasing susceptibility and infectiousness. Recent genital ulcers and higher levels of HIV in blood significantly increased the likelihood of transmission of HIV in these HIV-discordant couples (10, 11). Three rounds of mass treatment for bacterial STIs were given every 10 months in 56 communities in the rural Rakai district of Uganda from 1994 to 1997. The intervention trial resulted in a modest decrease in the prevalence of syphilis but no reduction in the incidence of HIV-1 (12). In the same setting, HSV-2 was identified as the cause of 45% of the genital ulcers that were tested and that had a confirmed etiology (12). Also, the HIV-1 epidemic in the Rakai district was at a mature stage, with a much higher prevalence of HIV-1 and a higher incidence of HIV-1 than that in the Mwanza region in the United Republic of Tanzania, where strengthened syndromic management of STDs reduced HIV incidence by 40% (12).
People who are co-infected with HIV and HSV-2 may experience more frequent episodes of genital herpes with symptomatic lesions and ulcers than people who are HIV-negative, which may also increase their risk of transmitting HIV-1 to others. The high prevalence of HSV-2 in all three sites of these community-randomized STD intervention trials indicates that genital herpes may be an important factor in explaining the different outcomes of the trials. This underscores the need for further trials to characterize the relationship that exists between HSV-2 and HIV transmission and to identify effective interventions. Interestingly, after patient education about genital herpes, 46 of the 53 asymptomatic persons did report lesions or other symptoms. The rate of subclinical shedding was similar in both groups, consistent with infection with genital herpes. HSV-2 was detected in the genital secretions of 44 of the 53 individuals in the group of HSV-2 seropositive subjects who did not report a history of genital herpes.
In general, the recurrent episodes in these subjects were shorter and less frequent than those reported in the group of 90 patients with known symptomatic disease. Shedding of HSV-2 was found to occur primarily in the anal and rectal region, and on almost half of the days on which HSV-2 was detected, no lesions were present.
As yet there are not enough data available to establish which diagnostic and treatment strategies, whether alone or in combination, will prove effective in reducing the prevalence of HSV-2 in developing countries.
HSV-2 intervention trials exploring episodic and suppressive therapy with acyclovir in developing countries are just beginning and will raise as many questions as they answer about the feasibility and implementation of programmes in countries with varying resources.
New WHO guidelines for the syndromic management of genital ulcer disease are likely to result in more people being diagnosed with and treated for HSV-2, although the overall impact on prevalence of HSV-2 and on HSV-2 and HIV transmission will not be evident for several years (4). For the minority of people who present with genital lesions, clinical diagnosis is unreliable because of the diverse and subtle symptoms of HSV-2 infection. Herpes ulcers often mimic other causes of genital ulcers, such as chancroid, another STI, and may be misdiagnosed even by experienced clinicians (18). Before these tests became available, no commercially available HSV antibody tests were able to differentiate between infection with HSV-1 (a related herpesvirus, most commonly associated with cold sores on the mouth) and HSV-2.
These new assays have acceptably high sensitivity and specificity for use in many settings, particularly in those with a high prevalence of infection (18). The HSV Western blot differentiates between antibodies to HSV-1 and HSV-2 and was developed more than a decade ago at the University of Washington, USA, but is not commercially available.
Although regarded as the gold standard for such tests, its high cost (US$ 95), the technical skill and experience required to conduct it, and the time needed for its performance prohibit its widespread use in developing countries (18). All serological assays have a time lag before antibodies are detectable after initial acquisition of HSV-2, the duration of which can range from several weeks up to several months (18). This vaccine is undergoing further evaluation and other candidate HSV-2 vaccines are at earlier stages of testing.
Traditionally, syndromic management has focused attention on chancroid and syphilis, two bacterial STIs that also cause genital ulcer disease, but that have declined in prevalence over the past decade. In areas such as sub-Saharan Africa, where the prevalence of HSV-2 is high, such approaches result in a lack of treatment for the most common cause of genital ulcer disease, i.e. The effect of HSV-2 therapy for the treatment of genital ulcer disease on people infected with HIV warrants study of HIV shedding during HSV-2 reactivation compared with that during suppression in relation to potential infectiousness. Several studies, including one funded by the US National Institutes of Health (NIH), are evaluating the efficacy of acyclovir in preventing the acquisition of HIV in HSV-2-infected individuals.
For the NIH trial, HIV-negative HSV-2-seropositive heterosexual women in South Africa, Zambia and Zimbabwe and homosexual men in Peru and the USA are being enrolled. The trial will provide data on the effect of twice-daily acyclovir suppressive therapy in preventing acquisition of HIV and data on adherence to suppressive acyclovir. The cost of implementing widespread suppressive therapy is difficult to justify in many developing countries. If the trial of suppressive HSV-2 therapy demonstrates reduced acquisition of HIV, suppressive therapy for people infected with HSV-2 could be targeted to those who are at high risk for HIV infection. The Bill and Melinda Gates Foundation has funded a trial of acyclovir suppressive therapy to reduce transmission of HIV in HIV-discordant couples in which the HIV-infected partner also has HSV-2 infection at a number of sites in Africa and India.

The approach needed may differ between areas depending on the stage of the HIV epidemic, the prevalence HSV-2 in high-risk populations, and on the cost and availability of diagnostic tests and treatment.
In countries in sub-Saharan Africa, where the prevalence of HSV-2 is extremely high, the provision of acyclovir for persons with genital ulcers who are being treated syndromically at clinics may be useful.
There are as yet too few data to determine which strategies will be most effective in which settings. The cost-effectiveness of providing HSV-2 suppressive therapy may be an important consideration; as with any intervention, the cost-effectiveness would be improved if it were possible to identify those individuals who would benefit most from HSV-2 suppression and to target suppressive therapy to them. The question of resistance to acyclovir developing as a result of its widespread use has been raised.
Also, the effect of episodic treatment of HSV-2 may not considerably shorten the duration of symptoms or HIV infectiousness in people co-infected with HIV and HSV, as there are often delays in seeking care and because treatment with antivirals results only in modest reductions in the duration of symptoms.
For these reasons, other strategies such as suppressive HSV-2 therapy, are actively being explored to reduce HIV infectiousness. While data were accumulating on the prevalence of HSV-2 infection and the role of HSV-2 in HIV acquisition and transmission, CDC did not have in place any recommendations or programmes specific to the prevention of genital herpes, apart from the standard STI treatment guidelines. In May 1998, CDC hosted a meeting of HSV-2 experts to define programmes to which it will be important to devote resources and to identify research priorities for CDC with regard to genital herpes (21). In these updated guidelines, CDC strongly recommended the use of laboratory tests for confirming the diagnosis of genital herpes and the use of accurate type-specific serological tests. Infection with HSV-2, even among people who do not have recognized herpes lesions, increases susceptibility to HIV, as documented by numerous observational studies.
HSV-2 also increases the risk of transmission of HIV, most likely through microulcerations and an increased amount of HIV in genital secretions during HSV-2 reactivation. In countries where there are large numbers of people infected with HSV-2 and HIV, suitable public health approaches for the diagnosis and management of genital herpes must be identified. Effective vaccines against HSV-2 have yet to be identified, and episodic and suppressive therapy approaches are often too expensive to be implemented in developing countries on a large scale. Although the epidemic of HSV-2 and the synergy between HSV-2 and HIV infection has been recognized by international public health experts, more research is needed to identify effective programmatic and clinical strategies for diagnosing and managing genital herpes worldwide. The authors would like to thank Neen Alrutz and David Stanton at USAID, Barbara de Zalduondo, Barbara Bever and Hilary Hughes at TvT, and Elaine Douglas, Ann Downer, King Holmes, Holly Huckeba and Amy Welton at the University of Washington for their invaluable help in creating the series. The Synergy Project is managed by TvT Global Health and Development Strategies, a division of Social and Scientific Systems, Inc.
The Center for Health Education and Research at the University of Washington is a subcontractor. Del Mar Pujades Rodríguez M, Obasi A, Mosha F, Todd J, Brown D, Changalucha J, et al. HIV infection among youth in a South African mining town is associated with herpes simplex virus-2 seropositivity and sexual behaviour.
The multicentre study on factors determining the differential spread of HIV in four African cities: summary and conclusions.
The epidemiology of HSV-2 infection and its association with HIV infection in four urban African populations.
Frequent recovery of HIV-1 from genital herpes simplex virus lesions in HIV-1-infected men. Probability of HIV-1 transmission per coital act in monogamous heterosexual, HIV-1-discordant couples in Rakai, Uganda.
Control of sexually transmitted diseases for HIV-1 prevention: understanding the implications of the Mwanza and Rakai trials.
Syndromic management of sexually-transmitted infections and behaviour change interventions on transmission of HIV-1 in rural Uganda: a community randomised trial.
Comparison of STD prevalence in the Mwanza, Rakai and Masaka trial populations: the role of selection bias and diagnostic errors.
Frequent genital herpes simplex virus 2 shedding in immunocompetent women: effect of acyclovir treatment. Reactivation of genital herpes simplex virus type 2 infection in asymptomatic seropositive persons. Herpes simplex virus shedding among human immunodeficiency virus-negative men who have sex with men: site and frequency of shedding. National Center for HIV, STD and TB Prevention, Division of Sexually Transmitted Diseases; 1998.

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