You are leaving Medscape Education
Cancel Continue
Log in to save activities Your saved activities will show here so that you can easily access them whenever you're ready. Log in here CME & Education Log in to keep track of your credits.
 

Table 1.  

Per-contact Probability in the HIV-1-Susceptible Partner
HIV-1 Plasma RNA in
Source Partner (copies/mL)
HSV-2 positive HSV-2 negative
<1700 0.0001 0.00004
1700-12,499 0.0023 0.0005
12,500-38,499 0.0018 0.0002
≥ 38,500 0.0036 0.0007

Table 1. Per-contact Probability of HIV-1 Infection in HSV-2-Seropositive and HSV-2-Seronegative Partners of HIV-1-Seropositive (Source) Subjects, Stratified by Plasma HIV-1 RNA Level of the Source Partner*[13]

*None of the source partners were treated with antiretroviral therapy.

Table 2.  

Women Men Total
Number of Patients Sampled* 132* 70 202
Number of days sampled 9098 4402 13,500
Median percent of days HSV detected (range) 16.6 (0-94.4) 12.1 (0-92) 15.0 (0-96.4)

Table 2. Frequency of HSV Reactivation as Measured by PCR Among Immunocompetent Men and Women[15]

* Persons sampled for > 30 days.

Table 3.  

Valacyclovir
(N = 743)
Placebo
(N = 741)
Total Hazard Ratio
(95% CI)
P
No. (%)
Acquisition of symptomatic HSV-2 infection 4 (0.5) 16 (2.2) 20 0.25 (0.08, 0.75) .008
Overall acquisition of HSV-2 infection 14 (1.9 ) 27 (3.6) 41 0.52 (0.27, 0.99) .04
Acquisition of HSV-1 or HSV-2 infections 14 (1.9) 31 (4.2) 45 0.45 (0.24, 0.84) .01

Table 3. Acquisition of HSV Infection Among Susceptible Partners, According to the Source Partner's Treatment Assignment*[19]

*P values were calculated using the log-rank test. CI denotes confidence interval.

Table 4.  

Hazard Ratio (95% CI)
Risk Univariate Adjusted*
Risk for each additional sex act per week 1.16 (1.05, 1.28) 1.16 (1.03, 1.30)
Condom use > 25% vs ≤ 25% 0.38 (0.11, 1.30) 0.25 (0.07, 0.88)
Sex when lesions present vs no sex when lesions present 2.01 (0.78, 5.18)
Acyclovir use by partner vs no acyclovir use 0.64 (0.24, 1.73)

Table 4. Effect of > 25% Condom Use on HSV-2 Acquisition[21]

*Adjusted estimates are from a model stratified by sex and adjusted for age, condom use, and sex acts per week.
CI, confidence interval; HR, hazard ratio; HSV-2, herpes simplex virus type 2

Table 5.  

Hazard Ratio
(95% CI)
P Adjusted Hazard Ratio*
(95% CI)
P
Condom use during study, ≤ 65% vs > 65% of sex acts 0.56
(0.33, 0.97)
.039 0.57
(0.33, 0.96)
.035

Table 5. Effect of > 65% Condom Use on HSV-2 Acquisition[22]

*Adjusted for age, race, and frequency of sexual activity.

Table 5.  

Hazard Ratio
(95% CI)
P Adjusted Hazard Ratio*
(95% CI)
P
Condom use during study, ≤ 65% vs > 65% of sex acts 0.56
(0.33, 0.97)
.039 0.57
(0.33, 0.96)
.035

Table 5. Effect of > 65% Condom Use on HSV-2 Acquisition[22]

*Adjusted for age, race, and frequency of sexual activity.

Clinical Tools for Preventing Sexual Transmission of Genital Herpes

Authors: Lawrence Corey, MDFaculty and Disclosures

processing....

Genital Herpes: A Worldwide Epidemic

Genital herpes is perhaps the most common sexually transmitted infection in the world. Herpes simplex virus type 2 (HSV-2) seroprevalence has significantly increased in the last 20 years: in almost all parts of the world, 20% to 60% of sexually active adult men and women have antibodies to HSV-2 (Figure 1).[1] In the United States, population-based studies have indicated that 22% of adults have antibodies to HSV-2 and that an estimated 1.6 million new cases of HSV-2 infection occur each year.[2,3] Further, with the advent of polymerase chain reaction (PCR) testing, it has become apparent that HSV-2 is the most frequent cause of genital ulcer disease in all regions of the world. Studies in India, the Republic of South Africa, Tanzania, and Thailand have shown that HSV-2 may be the cause of up to 80% of all genital ulcerations.[4-7] In the United States and Western Europe, the prevalence of HSV-2 as a cause of genital ulcerations may be even higher.[8]

Figure 1.

Enlarge

HSV-2 prevalence among women.[1]

Over the past decade, studies of the natural history of genital herpes have brought increasing recognition that HSV-2 causes chronic infection characterized by frequent reactivations in genital mucosa and the attendant risk of sexual transmission of infection. Significantly, both symptomatic and asymptomatic reactivations have been shown to result in sexual transmission of HSV-2.[9] Genital herpes reactivations have also been linked with the sexual transmission of other sexually transmitted infections, including human immunodeficiency virus type 1 (HIV-1) infection.

Mounting data describe an epidemiologic synergism between HSV-2 and HIV-1. HSV-2 prevalence appears to influence HIV incidence and vice versa.[10] A meta-analysis of data from more than 30 studies recently determined that the relative risk for HIV acquisition among persons with HSV-2 infection was 2.1 (95% confidence interval [CI], 1.4-3.2); using this estimate, the authors calculated the population-attributable risk percent (ie, the percentage of HIV infections attributable to genital herpes infection) to be 19% in populations with 22% HSV-2 prevalence, and 47% in populations with 80% HSV-2 prevalence -- a level existing in many parts of sub-Saharan Africa.[11] Similarly, a study of factors associated with differences in HIV transmission in cities with high and low HIV prevalence showed that high HSV-2 seroprevalence and low circumcision rates were major risk factors for the spread of HIV.[12] The most direct and compelling data regarding the link between HSV-2 infection and HIV-1 transmission were yielded by a retrospective analysis of factors associated with new HIV infections among HIV discordant couples in Rakai, Uganda.[13] This study found that a higher viral load in the HIV-infected partner and genital ulceration in the susceptible partner were the main determinants of HIV transmission. Specifically, HSV-2 seropositivity of the susceptible partner was found to increase the risk of HIV acquisition by 5- to 8-fold per sexual contact, regardless of the HIV viral load of the HIV infected partner ( Table 1 ). In fact, the per-contact sexual transmission rate from an HIV-positive partner with an HIV-1 RNA level of < 1500 RNA copies/mL to an HIV uninfected, HSV-2 seropositive partner was equal to that from an HIV-seropositive person with a viral load > 37,000 copies/mL to an HIV-negative, HSV-2-seronegative partner. In light of the widespread prevalence of HSV-2 infection, these findings illustrate, on a population basis, the dramatic effect that HSV-2 seropositivity has upon the spread of HIV.

These findings have brought about a fundamental shift in the medical establishment regarding the importance of preventing genital herpes infections, especially in populations at risk for HIV-1 infection.[14] This shift has finally placed the concerns of physicians and health officials in concert with those of patients with known genital herpes infections, a majority of whom for years have identified transmission of the infection to others as their chief concern regarding the disease.

Almost all new cases of genital herpes, however, are transmitted among persons who are unaware of their having HSV-2 infection, unaware of the importance of subclinical reactivation in the transmission of disease, and unaware of the mild clinical symptoms of HSV-2 and the attendant frequent reactivations that occur with HSV-2 seropositivity.[15] Table 2 depicts a compilation of data showing the frequency of HSV-2 reactivation as measured by PCR in various populations. While there is a wide range of variability between individuals, the median frequency of reactivation is quite high and illustrates the reason for the widespread epidemic of HSV-2 that is occurring worldwide.

Table of Contents

  1. Genital Herpes: A Worldwide Epidemic
  2. Preventing HSV-2 Transmission
  3. Conclusions
  • Print