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11 tips to help you manage your herpes.
There are a number of home remedies that you can use to help relieve your genital herpes symptoms . There is no cure for herpes , however, here are some beneficial tips to consider for herpes management :
Here are some tips to help you deal with any discomfort you may experience during an outbreak:
A genital herpes outbreak can be very distressing. Many sufferers of genital herpes experience stress, anxiety, and embarrassment as a result of suffering from this disease, and these feelings are exponential during the time of an outbreak. Like most viral conditions, stress and anxiety is a huge trigger.
Sufferers can avoid these feelings by adopting a few genital herpes home treatment tips that should help avoid outbreaks, and reduce the severity when outbreaks occur.
Herdox's potent formula works to enhance immunological functioning; helping to reduce HSV's most troublesome symptoms and reducing the number of outbreaks you have. Herdox is your natural means for effective and long-term HSV suppression.
The formula allows you to manage your condition in the privacy and security of your own home. Progressive Health has taken years of clinical research and developed the most effective, multi-faceted HSV supplement to date. Based on the anti-herpes nutrient L-lysine, Herdox's ingredients provide for significant improvements in immunological functioning.
Other remedies and drugs available for herpes:
For a complete list of ingredients Click Here .
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Recommended Regimens for Episodic Therapy for Recurrent HSV-2 Genital Herpes*
Recommended Regimens for Daily Suppressive Therapy Among Persons with HIV
Recommended Regimens for Episodic Infection Among Persons with HIV
Recommended Regimen for Suppression of Recurrent Genital Herpes Among Pregnant Women*

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Genital herpes is a chronic, lifelong viral infection. Two types of HSV can cause genital herpes: HSV-1 and HSV-2. Most cases of recurrent genital herpes are caused by HSV-2, and 11.9% of persons aged 14–49 years are estimated to be infected in the United States ( 436 ). However, an increasing proportion of anogenital herpetic infections have been attributed to HSV-1, which is especially prominent among young women and MSM ( 186 , 437 , 438 ).
The majority of persons infected with HSV-2 have not had the condition diagnosed, many of whom have mild or unrecognized infections but shed virus intermittently in the anogenital area. Consequently, most genital herpes infections are transmitted by persons unaware that they have the infection or who are asymptomatic when transmission occurs. Management of genital HSV should address the chronic nature of the infection rather than focusing solely on treating acute episodes of genital lesions.
Clinical diagnosis of genital herpes can be difficult because the self-limited, recurrent, painful, and vesicular or ulcerative lesions classically associated with HSV are absent in many infected persons at the time of clinical evaluation. If genital lesions are present, clinical diagnosis of genital herpes should be confirmed by type-specific virologic testing from the lesion by NAAT or culture ( 186 ). Recurrences and subclinical shedding are much more frequent for HSV-2 genital herpes infection than for HSV-1 genital herpes ( 439 , 440 ). Therefore, prognosis and counseling depend on which HSV type is present. Type-specific serologic tests can be used to aid in the diagnosis of HSV infection in the absence of genital lesions. Both type-specific virologic and type-specific serologic tests for HSV should be available in clinical settings that provide care to persons with or at risk for STIs. HSV-2 genital herpes infection increases the risk for acquiring HIV twofold to threefold; therefore, all persons with genital herpes should be tested for HIV ( 441 ).
HSV NAAT assays are the most sensitive tests because they detect HSV from genital ulcers or other mucocutaneous lesions; these tests are increasingly available ( 442 – 444 ). Although multiple FDA-cleared assays exist for HSV detection, these tests vary in sensitivity from 90.9% to 100%; however, they are considered highly specific ( 445 – 447 ). PCR is also the test of choice for diagnosing HSV infections affecting the central nervous system (CNS) and systemic infections (e.g., meningitis, encephalitis, and neonatal herpes). HSV PCR of the blood should not be performed to diagnose genital herpes infection, except in cases in which concern exists for disseminated infection (e.g., hepatitis). In certain settings, viral culture is the only available virologic test. The sensitivity of viral culture is low, especially for recurrent lesions, and decreases rapidly as lesions begin to heal ( 443 , 448 ). Viral culture isolates and PCR amplicons should be typed to determine whether HSV-1 or HSV-2 is causing the infection. Failure to detect HSV by NAAT or culture, especially in the presence of older lesions or the absence of active lesions, does not indicate an absence of HSV infection because viral shedding is intermittent. Similarly, random or blind genital swabs in the absence of lesions should not be used to diagnose genital HSV infection because sensitivity is low, and a negative result does not exclude the presence of HSV infection.
Cytologic detection of cellular changes associated with HSV infection is an insensitive and nonspecific method of diagnosing genital lesions (i.e., Tzanck preparation) and therefore should not be relied on. Although a direct immunofluorescence assay using fluorescein-labeled monoclonal antibodies is also available for detecting HSV antigen from genital specimens, this assay lacks sensitivity and is not recommended ( 449 ).
Both type-specific and type-common antibodies to HSV develop during the first weeks after infection and persist indefinitely. The majority of available, accurate type-specific HSV serologic assays are based on the HSV-specific glycoprotein G2 (gG2) (HSV-2) and glycoprotein G1 (gG1) (HSV-1). Type-common antibody tests do not distinguish between HSV-1 and HSV-2 infection; therefore, type-specific serologic assays should be requested ( 450 – 452 ).
Both laboratory-based assays and POC tests that provide results for HSV-2 antibodies from capillary blood or serum during a clinic visit are available. The sensitivity of glycoprotein G type-specific tests for detecting HSV-2 antibody varies from 80% to 98%; false-negative results might be more frequent at early stages of infection ( 451 , 453 , 454 ). Therefore, in cases of recent suspected HSV-2 acquisition, repeat type-specific antibody testing 12 weeks after the presumed time of acquisition is indicated. The most commonly used test, HerpeSelect HSV-2 enzyme immunoassay (EIA), often is falsely positive at low index values (1.1–3.0) ( 457 – 457 ). One study reported an overall specificity of 57.4%, with a specificity of 39.8% for index values of 1.1–2.9 ( 458 ). Because of the poor specificity of commercially available type-specific EIAs, particularly with low index values (<3.0), a confirmatory test (Biokit or Western blot) with a second method should be performed before test interpretation. Use of confirmatory testing with the Biokit or the Western blot assays have been reported to improve accuracy of HSV-2 serologic testing ( 459 ). The HerpeSelect HSV-2 immunoblot should not be used for confirmation because it uses the same antigen as the HSV-2 EIA. If confirmatory tests are unavailable, patients should be counseled about the limitations of available testing before obtaining serologic tests, and health care providers should be aware that false-positive results occur. Immunoglobulin M (IgM) testing for HSV-1 or HSV-2 is not useful because IgM tests are not type specific and might be positive during recurrent genital or oral episodes of herpes ( 460 ). Therefore, HSV IgM testing is not recommended.
Because approximately all HSV-2 infections are sexually acquired, presence of type-specific HSV-2 antibody implies anogenital infection. In this instance, education and counseling for persons with genital HSV infections should be provided. The presence of HSV-1 antibody alone is more difficult to interpret. HSV-1 serologic testing does not distinguish between oral and genital infection and typically should not be performed for diagnosing genital HSV-1 infection. Persons with HSV-1 antibodies often have oral HSV infection acquired during childhood, which might be asymptomatic. Lack of symptoms in a person who is HSV-1 seropositive does not distinguish anogenital from orolabial or cutaneous infection, and, regardless of site of infection, these persons remain at risk for acquiring HSV-2. In addition, HSV-1 serologic testing has low sensitivity for detection of HSV-1 antibody ( 458 ). However, acquisition of HSV-1 genital herpes is increasing, and HSV-1 genital herpes also can be asymptomatic ( 437 – 439 , 461 , 462 ). Diagnosis of HSV-1 infection is confirmed by virologic tests from genital lesions.
Type-specific HSV-2 serologic assays for diagnosing HSV-2 are useful in the following scenarios: recurrent or atypical genital symptoms or lesions with a negative HSV PCR or culture result, clinical diagnosis of genital herpes without laboratory confirmation, and a patient’s partner has genital herpes. HSV-2 serologic screening among the general population is not recommended. Patients who are at higher risk for infection (e.g., those presenting for an STI evaluation, especially for persons with ≥10 lifetime sex partners, and persons with HIV infection) might need to be assessed for a history of genital herpes symptoms, followed by type-specific HSV serologic assays to diagnose genital herpes for those with genital symptoms.
Antiviral medication offers clinical benefits to symptomatic patients and is the mainstay of management. The goals for use of antiviral medications to treat genital herpes infection are to treat or prevent symptomatic genital herpes recurrences and improve quality of life and suppress the virus to prevent transmission to sexual partners. Counseling regarding the natural history of genital herpes, risks for sexual and perinatal transmission, and methods for reducing transmission is also integral to clinical management.
Systemic antiviral drugs can partially control the signs and symptoms of genital herpes when used to treat first clinical and recurrent episodes or when used as daily suppressive therapy. However, these drugs neither eradicate latent virus nor affect the risk, frequency, or severity of recurrences after the drug is discontinued. Randomized trials have indicated that three FDA-approved antiviral medications provide clinical benefit for genital herpes: acyclovir, valacyclovir, and famciclovir ( 463 – 471 ). Valacyclovir is the valine ester of acyclovir and has enhanced absorption after oral administration, allowing for less frequent dosing than acyclovir. Famciclovir also has high oral bioavailability. Topical therapy with antiviral drugs offers minimal clinical benefit and is discouraged.
Newly acquired genital herpes can cause a prolonged clinical illness with severe genital ulcerations and neurologic involvement. Even persons with first-episode herpes who have mild clinical manifestations initially can experience severe or prolonged symptoms during recurrent infection. Therefore, all patients with first episodes of genital herpes should receive antiviral therapy.
Acyclovir† 400 mg orally 3 times/day for 7–10 days
OR
Famciclovir 250 mg orally 3 times/day for 7–10 days
OR
Valacyclovir 1 gm orally 2 times/day for 7–10 days
* Treatment can be extended if healing is incomplete after 10 days of therapy.
†Acyclovir 200 mg orally five times/day is also effective but is not recommended because of the frequency of dosing.
Almost all persons with symptomatic first-episode HSV-2 genital herpes subsequently experience recurrent episodes of genital lesions. Intermittent asymptomatic shedding occurs among persons with HSV-2 genital herpes infection, even those with longstanding clinically silent infection. Antiviral therapy for recurrent genital herpes can be administered either as suppressive therapy to reduce the frequency of recurrences or episodically to ameliorate or shorten the duration of lesions. Certain persons, including those with mild or infrequent recurrent outbreaks, benefit from antiviral therapy; therefore, options for treatment should be discussed. Many persons prefer suppressive therapy, which has the additional advantage of decreasing the risk for transmitting HSV-2 genital herpes to susceptible partners ( 472 , 473 ).
Suppressive therapy reduces frequency of genital herpes recurrences by 70%–80% among patients who have frequent recurrences ( 469 – 472 ). Persons receiving such therapy often report having experienced no symptomatic outbreaks. Suppressive therapy also is effective for patients with less frequent recurrences. Long-term safety and efficacy have been documented among patients receiving daily acyclovir, valacyclovir, and famciclovir ( 474 ). Quality of life is improved for many patients with frequent recurrences who receive suppressive therapy rather than episodic treatment ( 475 ). Providers should discuss with patients on an annual basis whether they want to continue suppressive therapy because frequency of genital HSV-2 recurrence diminishes over time for many persons. However, neither treatment discontinuation nor laboratory monitoring is necessary because adverse events and development of HSV antiviral resistance related to long-term antiviral use are uncommon.
Treatment with valacyclovir 500 mg daily decreases the rate of HSV-2 transmission for discordant heterosexual couples in which a partner has a history of genital HSV-2 infection ( 473 ). Such couples should be encouraged to consider suppressive antiviral therapy as part of a strategy for preventing transmission, in addition to consistent condom use and avoidance of sexual activity during recurrences. Suppressive antiviral therapy for persons with a history of symptomatic genital herpes also is likely to reduce transmission when used by those who have multiple partners. HSV-2 seropositive persons without a history of symptomatic genital herpes have a 50% decreased risk for genital shedding, compared with those with symptomatic genital herpes ( 476 ). No data are available regarding efficacy of suppressive therapy for preventing HSV-2 transmission among discordant couples in which a partner has a history of asymptomatic HSV-2 infection identified by a positive HSV-2 serologic test. Among HSV-2 seropositive persons without HIV infection, oral TDF/FTC and intravaginal tenofovir are ineffective at reducing the risk for HSV-2 shedding or recurrences ( 477 ).
Acyclovir 400 mg orally 2 times/day
OR
Valacyclovir 500 mg orally once a day*
OR
Valacyclovir 1 gm orally once a day
OR
Famciclovir 250 mg orally 2 times/day
* Valacyclovir 500 mg once a day might be less effective than other valacyclovir or acyclovir dosing regimens for persons who have frequent recurrences (i.e., ≥10 episodes/year).
Famciclovir appears somewhat less effective for suppression of viral shedding ( 478 ). Ease of administration and cost also are key considerations for prolonged treatment.
Recurrences are less frequent after the first episode of HSV-1 genital herpes, compared with genital HSV-2 genital herpes, and genital shedding rapidly decreases during the first year of infection ( 479 ). No data are available regarding the efficacy of suppressive therapy for preventing transmission among persons with HSV-1 genital herpes infection. Because of the decreased risk for recurrences and shedding, suppressive therapy for HSV-1 genital herpes should be reserved for those with frequent recurrences through shared clinical decision-making between the patient and the provider.
Episodic treatment of recurrent herpes is most effective if therapy is initiated wi
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