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Basic Fact Sheet Detailed Version. Detailed fact sheets are intended for physicians and individuals with specific questions about sexually transmitted diseases. Detailed fact sheets include specific testing and treatment recommendations as well as citations so the reader can research the topic more in depth. Genital herpes infection is common in the United States.

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Herpes simplex virus HSV -2 is periodically shed in the human genital tract, most often asymptomatically, and most sexual transmissions occur during asymptomatic shedding. It would be helpful to identify a genital viral load threshold necessary for transmission, as clinical interventions that maintain viral quantity below this level would be of high utility.

However, because viral expansion, decay and re-expansion kinetics are extremely rapid during shedding episodes, it is impossible to directly measure genital viral load at the time of sexual activity.

We developed a mathematical model based on reproducing shedding patterns in transmitting partners, and median of sex acts prior to transmission in discordant couples, to estimate infectivity of single viral particles in the negative partner's genital tract. We then inferred probability estimates for transmission at different levels of genital tract viral load in the transmitting partner.

Moreover, most transmissions occur during prolonged episodes with high viral copy s. Many shedding episodes that result in transmission do not reach the threshold of clinical detection, because the ulcer remains very small, highlighting one reason why HSV-2 spre so effectively within populations. HSV-2 shedding consists of frequent episodes approx. Transmission to an uninfected partner occurs following coitus during genital shedding in an infected person.

Accordingly, data from persons with newly acquired HSV-2 suggest that the of coital acts prior to transmission is quite low [ 7 ]. Antiviral therapies or immunotherapies that more effectively maintain HSV-2 shedding below a certain level may be valuable for decreasing HSV-2 incidence.

In murine models of infection, a threshold inoculum dose of HSV is needed to ensure infection [ 12 ]. Breakthrough shedding occurs in aciclovir- and valaciclovir-treated patients, explaining this intervention's incomplete efficacy [ 14 ]. Yet, there is room for optimism: for human immunodeficiency virus HIV -1, another viral sexually transmitted infection, whereas probability of transmission increases as a function of genital and plasma tract viral load [ 1516 ], control of HIV-1 replication with potent antiretroviral therapy virtually abrogates transmission [ 17 ]. Unfortunately, although finely detailed descriptions of HSV-2 shedding are available, it is impossible to measure viral load at the time of transmission: clinical sampling is not Seeking a woman hsv2 24 35 performed immediately prior to coitus, and viral quantities in the genital tract can vary fold over the course of hours, making next day measurement unreliable [ 18 ].

However, viral quantity at coitus is likely to predict the probability of a virus contacting and engaging receptors on susceptible cells in the uninfected partner's genital tract. It is highly likely that viral load has at least a partially predictive relationship on probability of transmission. We therefore deed mathematical models of HSV transmission to estimate a conservative threshold genital viral load for transmission. The model's output generates transmission probability curves based on viral load at the time of coitus. Moreover, the model demonstrates how asymptomatic shedding le to many transmissions, even though shedding during visible lesions has a higher viral copy .

Genital herpes - cdc fact sheet (detailed)

We deed a biological transmission model that consists of two mechanistic components: shedding in the transmitting, HSVpositive partner and acquisition in the uninfected partner figure 1. We used a ly published model to reproduce genital viral shedding in the transmitter [ 18 ]. This stochastic, spatial model see Methods closely reproduces patterns of shedding established in study participants [ 1 ].

The percentage of swabs within 0. The model reproduces this frequency histogram of shedding at different viral lo, as well as rate, expansion and decay kinetics, peak viral quantity, and complex morphology of heterogeneous shedding episodes [ 18 ]. Schematic of the transmission model.

Equations table 1 describe shedding in an infected partner, transfer of cell-free virions to the uninfected partner during coitus, and infection, which occurs when a virus enters and replicates within an epithelial cell in the uninfected person. Frequency histogram of quantitative shedding.

Data are from study participants who submitted 14 genital swabs. When transmission occurred one or more cells became infectedfeatures of the episode leading to transmission were recorded. We therefore used estimates for the median of acts prior to transmission to arrive at a value for viral infectivity, and then used an estimate of viral infectivity to estimate of acts prior to transmission, to see if these processes produced consistent .

The most rigorous available estimate for median acts prior to transmission is 40 inter-quartile range IQR : 15—75 : these data are from a retrospective study in which newly infected participants estimated the of coital acts prior to acquisition in new, exclusive partnerships. Participants had only one HSVinfected sexual partner in the time period leading up to transmission [ 7 ].

Because condom use is partly protective against HSV-2 transmission and acquisition [ 2021 ], and most transmissions occur when the at-risk member of a relationship is unaware of their partner's HSV-2 infection [ 7 ], the conditions in the retrospective cohort study reflect those that drive the HSV-2 epidemic in the general population. Given the cumulative probability distribution 0. If we assumed 15 and 75 median acts prior to transmission to establish reasonable bounds for the per coital act risk based on the IQR in [ 7 ]then the per coital act risk was 4.

If the risk was less than 0.


Conversely, under the assumption that all shedding during sex in transmission regardless of viral load, a median of 3. Per coital act risk assessment. Coloured dots represent different estimates of transmission risk. Orange, red and blue are estimates for the median of acts prior to transmission red, median 40 acts; orange and blue, lower and upper IQR 15 and 75 acts, respectively from a retrospective cohort study of acute infection [ 7 ]. Line colours correlate with dot colours in a.

Model estimates for per particle infectivity.

Each circle represents from simulations at the given parameter. Boxes represent IQR and whiskers represent all values within 1. Simulations with low, medium and high infectivity are used in the remainder of the article to estimate plausible ranges of viral load thresholds for transmission.

Given this estimate of infectivity, the risk of HSV-2 transmission per sex act was 2. This per coital act estimate is 0. Next, we conducted transmission simulations assuming low, medium and high infectivity, and identified skewed distributions of the of acts prior to transmission under each assumption figure 4 b.

For medium infectivity, while the median of acts before transmission was 40, there was considerable variability IQR: 19—61, range: 1— of acts preceding transmission can be high within a minority of discordant couples despite a constant per coital act risk. This effect was most pronounced with decreasing viral infectivity, which substantially widened both the IQR and total range figure 4 b. To demonstrate model output, we plotted four simulated transmissions and included: coital acts, genital tract viral load and lesion diameter.

A fundamental feature of empirical and model generated shedding episodes is their diversity. Episodes with higher copy have more infected cells and, in turn, larger ulcer diameter.

In addition, their morphology is often notable for multiple peaks figure 5 a—d. In simulated transmissions, most coital acts occurred when shedding was absent. This ed for prolonged time before transmission during certain simulations. Non-transmission coital acts are denoted with green lines; transmission coital acts are denoted with blue lines; HSV DNA copies is shown with a red line and peak lesion diameter with a purple line. We recorded genital viral load during each simulated coital act during transmissions at varying levels of infectivity.

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At medium infectivity, the median log 10 genital viral load during coital acts that resulted in transmission was 7. Only three 0. At low infectivity, median log 10 genital viral load during coital acts with transmission was higher: 7. At higher infectivity, median genital viral load during coital acts with transmission was lower: 6. Genital tract viral load is a predictor of transmission.

To reinforce our estimates of viral load transmission threshold, we constructed a statistical risk model see Methodswhich we fitted to ly obtained data on the of sex acts prior to transmission [ 7 ]. The model assumes a transmission risk associated with each coital event. Unlike the mechanistic mathematical model figure 1the statistical model ignores characteristics of shedding episodes figure 5. This estimate was 2. Therefore, if more confounding variables are assumed to impact transmission, then transmission probability at lower viral lo will be higher, whereas transmission probability at higher viral lo will be lower figure 6 d.

We next reverted to the simulation model figure 1 to classify type of episodes associated with transmissions, by performing further analyses on the simulated transmissions with an assumption of medium infectivity. We allowed episodes to be counted multiple times to for multiple coital acts during single episodes.

Viral lo in the genital tract fluctuated over hours and transmission did not usually occur at viral peaks within episodes: median peak log 10 viral load of transmission episodes was 7.

Median copy of 15 non-coital episodes was 2. Transmission episode duration was also longer than duration of coital and non-coital episodes figure 7 b. Severe shedding episodes as a predictor of transmission. All simulations assume medium infectivity. Distribution of c peak viral lo and d episode durations in simulated episodes.

The relative dearth of non-coital episodes with peak viral load between log 10 HSV DNA copy 4 and 6, as well as duration between 0 and 10 days, demonstrates a fundamental feature of both empirical and simulated shedding data. We estimated lesion diameter with our spatial model by counting the of missing cells owing to cell death within a single herpetic ulcer [ 1922 ]. For the simulated transmissions, the median diameter of the largest ulcer at the time of transmission was 2. Therefore, simulated transmissions often occurred when the lesion had not yet, or had already, achieved its maximum diameter.

Twenty-four per cent of transmission episodes occurred with more than 10 6 HSV DNA copies present despite no ulcer wider than 2 mm figure 8 b.

Herpes simplex virus-2 transmission probability estimates based on quantity of viral shedding

Many transmissions occurred at time points early during episodes prior to detectable lesions figure 8 c. Many transmissions occur when viral load is high but lesions are not visible. Data from transmission episodes. To forecast the effect of therapy on the risk of HSV-2 transmission, we simulated shedding on several dosing regimens of aciclovir and valaciclovir [ 1423 ].