Genital herpes is a sexually transmitted disease caused by herpes simplex virus (HSV) infection of the skin and mucous membranes of the genital and anal regions of the urinary tract. HSV can be divided into type 1 (HSV-1) and type 2 (HSV-2), and genital herpes is mainly caused by HSV-2, but can also be caused by HSV-1 or a mixture of both types. Epidemiology Seroepidemiological surveys and clinical case reports have shown a significant increase in the incidence of the disease, but it is difficult to accurately assess the prevalence of the disease in China due to factors such as survey methods, survey population and subclinical infections and atypical presentations. The disease is mainly transmitted through direct skin/mucous membrane contact, and infection by other means is extremely unlikely; therefore, unsafe sex is a high risk factor for the development of the disease. The risk of co-infection with HIV has been clinically found to be significantly higher in the population of patients with genital herpes, which may be related to the disruption of the skin-mucosal barrier caused by the former or the existence of complex interactions between the two viruses. In recent years, there has been an increase in genital herpes caused by HSV-1 infection, which may be related to changes in sexual behavior. III. Clinical manifestations Genital herpes can be divided into primary, recurrent, and subclinical HSV-activated types, and in addition there are some special types with their own characteristics of clinical manifestations. (A) primary episode of genital herpes (first episode of genital herpes): the first clinical manifestations, including primary genital herpes (primary genital herpies) (HSV infection for the first time) and non-primary primary genital herpes (previous HSV infection). The incubation period is usually 2 to 14 days, and patients generally have a long duration of illness, which can last 5 to 20 days. The disease is severe and can be combined with systemic symptoms (such as fever, headache, general malaise and muscle aches). The affected area is erythematous in the early stages and rapidly develops into blisters, erosions and ulcers, with significant local pain, and increased vaginal discharge in women due to involvement of the cervix. In some patients, the lesions are more extensive and can occur outside the genital area. (b) Recurrent genital herpes: Most cases can develop into recurrent genital herpes. Systemic symptoms are rare, lesions are limited, and the duration of the disease is relatively short, usually lasting 6-10 days. The frequency of recurrence varies greatly among individuals, with an average of 3 to 4 times/year, and frequent episodes can exceed 10 times per year. 1. Typical manifestations: Most of them have prodromal symptoms such as local itching, burning, tingling, vague pain, numbness and perineal swelling a few hours to 5 days before the onset of the rash, followed by clustered small blisters, which soon break down to form vesicles or superficial ulcers, with lighter self-conscious symptoms than the initial ones, lasting 6 to 10 days before healing. 2.Typical manifestations: It may show non-specific limited erythema, punctate erosion, fissure, ulcer, exudation, hard nodules (or boils) and folliculitis, etc., which need to be distinguished from other diseases. (iii) Subclinical reactivation of HSV: HSV is activated in the body without clinical manifestations, but can be intermittently detoxified. Viral activation can occur in multiple anatomical sites (e.g., vagina, cervix, rectum, etc.), and the virus can be isolated from a normal-looking involved site. The greatest risk in patients with subclinical HSV activation is that of infectious partners. Studies have shown that 70% of transmission occurs after sexual contact in patients with subclinical HSV activation, and that women are more likely to be infected. (d) special types of genital herpes: 1, neonatal herpes: can be divided into limited, central nervous system type and disseminated type, for the serious type of the disease, almost always infected by contact through the birth canal during childbirth, can endanger the life of the child. 2. Herpetic cervicitis: manifests as mucopurulent cervicitis, which can present with cervical congestion, increased fragility, blistering, mucosal erosion and even necrosis. 3, herpes proctitis: mostly seen in men who have sex with men, can be manifested as perianal blisters, ulcers, self-conscious pain, can also be manifested as urgency, constipation and rectal mucus bloody discharge, often accompanied by fever, general malaise, myalgia, etc. The sensitivity is related to the different lesion patterns such as erythema, blisters and crusts, and the success rate of viral culture is relatively high for blisters. Since the viral load of primary genital herpes is much higher than that of recurrent, its viral culture success rate is also higher. 2. Antigen detection: HSV antigen can be detected using enzyme-linked immunosorbent assay or immunofluorescence test, but the virus type cannot be distinguished. When HSV infection is suspected but no lesions or lesions are atypical, antigen detection can be used to identify subclinical HSV activation or atypical genital herpes. 3, nucleic acid detection: PCR can detect HSV-DNA, its significance is similar to the antigen test, but more sensitive, because its application in the clinic is limited by equipment, price and false positive problems, less routinely carried out. 4, serum antibody detection: ELISA or Western blot test can detect serum medium-sized specific antibodies, and can be used to distinguish the virus type. However, because serological testing is influenced by a variety of factors such as infection status and methodology, antibody testing is only used as clinical supporting diagnostic evidence for genital herpes, combined with comprehensive clinical analysis, and cannot be used alone as a basis for confirming or excluding the diagnosis. At present, antibody testing is mostly used for epidemiological investigation and retrospective clinical analysis. V. Diagnosis 1. Diagnostic criteria: clinical diagnostic criteria: history of unsafe sex, self or sexual partner infection, and typical clinical manifestations, atypical lesions need to be combined with pathogenic examination to confirm the diagnosis. Pathogenic diagnostic criteria: clinical diagnostic criteria plus positive pathogenic examination results. In addition, certain skin diseases (such as herpes zoster, contact dermatitis, fixed drug rash, pyoderma, Reiter’s disease, candidiasis, etc.) may also cause similar manifestations and require clinical attention. (i) Treatment goals: relief of symptoms, reduction of recurrence, reduction of detoxification, and reduction of psychological burden on the patient. (b) Patient education: HSV-2 infection is more likely to recur than HSV-1 infection, but there is a tendency for recurrence to decrease in some patients as the duration of disease increases. Regular lifestyle habits, appropriate physical exercise and good psychological status should be maintained. Excessive alcohol consumption, fatigue, cold, anxiety and tension are common triggers for genital herpes recurrence. For the health of the sexual partner and to reduce cross-contamination, the necessary preventive measures should be taken in a timely manner, and the disease suggests that the sexual partner be examined and treated as soon as possible. For pregnant patients, there is no clear evidence to confirm that HSV can infect the fetus through blood or amniotic fluid. (iii) Systemic therapy: mainly antiviral therapy, divided into two kinds of intermittent therapy and long-term suppressive therapy. For patients with subclinical HSV activation, reasonable antiviral therapy can be given according to the specific situation, especially the patient’s own needs. 1. Intermittent therapy: i.e., antiviral drugs are given during an attack. It is recommended to start the medication within 24h of the appearance of prodromal symptoms or lesions. Options include: oral acyclovir 200mg 5 times daily for 5 days; or acyclovir 400mg 3 times daily for 5 days; or valacyclovir 500mg 2 times daily for 5 days; or valacyclovir 300mg 2 times daily for 7 days; or famciclovir 250mg 3 times daily for 5 days. For primary genital herpes, the treatment dose remains the same and the course of treatment is extended to 10 days. 2. Long-term suppressive therapy: For patients with frequent episodes, long-term suppressive therapy can be recommended for a duration of 6 months or longer, depending on patient needs and efficacy. There is no evidence that long-term suppressive therapy can prevent relapse after discontinuation. Options include: oral acyclovir 400mg twice daily; or valacyclovir 500mg once daily. 3. Treatment of special populations: (1) Neonatal herpes: HSV infection in neonates, especially disseminated infection, should be treated with early intravenous antiviral therapy, such as acyclovir (5 mg/kg each time) every 8 hours. After the symptoms are controlled, oral therapy can be considered for maintenance. (2) Herpes in pregnancy: The use of antiviral therapy in pregnant women should be weighed against the pros and cons and requires informed consent from the patient. Drug options include acyclovir and valacyclovir, both of which have no evidence of teratogenicity. In pregnant women with initial genital herpes, oral acyclovir 400 mg three times daily is recommended, and intravenous acyclovir should be administered if there are serious complications that may be life-threatening. Pregnant women with frequent recurrent or recent infections may be given continuous oral acyclovir during the last 4 weeks of pregnancy to reduce active damage and decrease local viral load, thereby reducing cesarean delivery rates. Pregnant women with a previous history of recurrent genital herpes but no signs of recurrence near term may undergo cesarean section before rupture of membranes if not contraindicated, but cesarean section does not completely prevent the development of neonatal herpes. A mother without active lesions may deliver vaginally, but the newborn should be monitored closely and treated promptly if suspicious manifestations are detected. (3) People with co-infection with HIV: The same treatment strategy as the general population infection. Long-term suppressive therapy is preferred for those with frequent episodes, but drug resistance should be a concern. (4) Local treatment: Keep the affected area locally clean and dry, use physiological sodium chloride solution, 3% boric acid solution, etc. to clean or wet compress, if there is no obvious exudation, topical application of 3% acyclovir cream, 1% penciclovir cream, etc. The prevention of genital herpes: (a) prevention of sexual partners and the general population: the source of infection includes patients with current disease, subclinical or asymptomatic detoxification patients, because the latter two are more insidious, so it is more important in clinical terms. Avoid unsafe sex and treat the patient’s sexual partners promptly. (b) Prevention of neonatal infection: Pregnant women with recurrent genital herpes or early gestational infection have a low risk of neonatal infection, while those with primary genital herpes occurring in late gestation have a higher risk of neonatal infection; therefore, the key factor in reducing the risk of neonatal infection is the prevention of HSV infection in pregnant women in late gestation. The key factor in reducing the risk of neonatal infection is to prevent HSV infection in the second trimester. If infection occurs in the second trimester (especially within 4 weeks before delivery), cesarean delivery or prophylactic treatment with acyclovir (acyclovir 5 mg/kg IV every 8 hours for 10-21 days) is recommended.