Genital herpes (GH) is a sexually transmitted disease (STD) caused by the herpes simplex virus (HSV), which infects the urogenital and perianal skin and mucosa. Antiviral treatments can shorten the duration of symptoms and signs in primary infections but are unable to completely eliminate the latent infection of HSV within the body, resulting in recurrent episodes of the disease.
Related Factors for Disease Onset
HSV is a double-stranded DNA virus and is divided into two serotypes: HSV-1 and HSV-2. Most cases of genital herpes are caused by HSV-2 infection. After invading the body, HSV is transported retrogradely into sensory ganglia, where it remains latent for a long period, primarily in the sacral ganglia.
Modes of Transmission
HSV is present in the exudate of skin lesions, cervical and vaginal secretions, semen, and prostatic fluid. Transmission occurs primarily through sexual contact. Pregnant women with primary HSV infection can transmit the virus to the fetus via the placenta or the cervix, leading to intrauterine infection. Neonates may acquire HSV infection in utero, during passage through the birth canal, or through postpartum contact, with the majority of perinatal infections occurring during delivery via the birth canal.
Effects on Mother and Child
Primary HSV infection during early pregnancy rarely leads to miscarriage or stillbirth. Late-pregnancy primary infections may be associated with preterm labor and fetal growth restriction. Severe cases of intrauterine infection are rare.
Clinical Manifestations
Genital herpes is classified into three types: primary, recurrent, and subclinical.
Primary Genital Herpes
Patients who exhibit clinical manifestations for the first time are classified as having primary genital herpes, which includes true primary genital herpes (initial HSV infection) and non-primary first-episode genital herpes (previously infected with another HSV type). Lesions typically present as clustered or scattered vesicles on the genital and anal skin, which erode or ulcerate after rupture and then crust over, healing spontaneously. Pain is often reported. Systemic symptoms, including inguinal lymphadenopathy, fever, headache, and fatigue, are often present.
Recurrent Genital Herpes
The first recurrence usually occurs 1–4 months after the primary infection, with lesions appearing at the original site. Lesions resemble those in primary genital herpes but are generally milder. Prodromal symptoms, such as localized burning, tingling, or dysesthesia, are frequently reported before the onset of skin lesions.
Subclinical Genital Herpes
Atypical lesions, such as small cracks or ulcers on the genital area, are the primary features in subclinical genital herpes. This type is most common and serves as a significant source of transmission. Nearly 50% of individuals infected with HSV-1 and 70%–80% of those infected with HSV-2 lack typical clinical symptoms.
Diagnosis and Differential Diagnosis
Because clinical features are non-specific, diagnosis relies on laboratory tests. Laboratory evaluations include:
Nucleic Acid Testing
Testing for HSV DNA in skin lesion samples, blood, cerebrospinal fluid, and cervical secretions improves diagnostic sensitivity and allows for virus typing.
Viral Culture
Culturing the virus from lesion samples enables typing and drug susceptibility testing, but this method is less commonly used due to its difficulty.
Antigen Detection
Direct immunofluorescence or enzyme-linked immunosorbent assays (ELISA) are used to detect HSV antigens in lesion samples and represent a commonly used rapid diagnostic method in clinical settings.
Serological Testing
ELISA is used to detect specific HSV IgG and IgM in serum or neonatal umbilical cord blood to evaluate the mother's infection status. Positive IgM in umbilical cord blood indicates intrauterine infection.
Differential diagnosis is required to distinguish genital herpes from syphilitic chancre, chancroid, herpes zoster, Behçet’s disease, and drug eruptions.
Treatment
Primary Infection
Antiviral treatment is initiated as soon as possible, ideally within 72 hours of lesion onset. Treatment options include:
- Acyclovir 0.2 g orally, five times daily, for 7–10 days; or 0.4 g orally, three times daily, for 7–10 days.
- Famciclovir 0.25 g orally, three times daily, for 7–10 days; or valacyclovir 0.5 g orally, twice daily, for 7–10 days.
Recurrent Infection
Treatment includes episodic therapy during flare-ups and long-term suppressive therapy. Episodic therapy involves starting antiviral treatment within 24 hours after the onset of symptoms during a recurrence. Options include:
- Acyclovir 0.8 g orally, twice daily, for 5 days; or 0.4 g orally, three times daily, for 5 days.
- Famciclovir options: 1 g orally, twice daily, for 1 day; or 0.5 g orally once, followed by 0.25 g orally, twice daily, for 2 days; or 0.125 g orally, twice daily, for 5 days.
- Valacyclovir 0.5 g orally, twice daily, for 3 days; or 1 g orally, once daily, for 5 days.
Patients with frequent recurrences (≥6 episodes per year) may benefit from long-term suppressive therapy. The typical duration of suppressive therapy is 4–12 months. Options include:
- Acyclovir 0.4 g orally, twice daily; or famciclovir 0.25 g orally, twice daily; or valacyclovir 0.5 g orally, once daily.
Treatment During Pregnancy
Although some infections are self-limiting, treatment can help alleviate symptoms, shorten the disease duration, and reduce infectivity. Safety data for the use of acyclovir during early pregnancy are limited and require further evidence. Acyclovir 0.4 g orally, three times daily, for 7–10 days is an option; if incomplete resolution occurs after 10 days, treatment may be extended. Starting at 36 weeks of gestation, continuous antiviral treatment with acyclovir is recommended until delivery to suppress viral replication.
Management During Labor
For pregnant women with a history of genital herpes, viral culture or PCR testing of suspicious lesions is performed before delivery. Serum IgG and IgM antibody levels are suggested for quantification at 35–36 weeks of gestation.
For those with active genital herpes lesions or prodromal symptoms, cesarean delivery is recommended. A history of genital herpes without active lesions at delivery does not constitute an indication for cesarean delivery.
Invasive procedures during labor, such as artificial rupture of membranes, use of scalp electrodes, vacuum extraction, or forceps-assisted delivery, are avoided to reduce neonatal exposure to HSV.
For mothers with active HSV infections, breastfeeding is considered safe if the breast has no active lesions; strict hand hygiene is essential.
During breastfeeding, the use of famciclovir is contraindicated, while acyclovir and valacyclovir are to be used with caution.
Follow-Up
Assessment of the need for continued suppressive antiviral therapy is recommended annually. The frequency of recurrences is expected to decrease over time, regardless of whether antiviral therapy is used.