Herpes simplex virus (HSV-1, HSV-2) infections are ubiquitous worldwide and have been described clinically since the 1700s. They usually present as painful vesicles on the skin and mucous membranes but may present as a disseminated infection. It has been reported that over 90% of adults have antibodies to HSV-1 and over 25% have antibodies to HSV-2. Transmission of the virus is through infected secretions: HSV-1, through contact with oral secretions (oral-facial herpes) and HSV-2, through contact with genital secretions (genital herpes); however, both HSV-1 and HSV-2 can cause genital and oral-facial infections. The virus can be transmitted from active lesions or shed from asymptomatic individuals. Recurrent infections usually indicate a reactivation of the initial virus, but reinfection is possible. Reactivation appears to be triggered by ultraviolet light, fever, menstruation, emotional stress, immunosuppression, infections by other organisms, and trauma to the skin or ganglia. Disseminated herpes infections in neonates and the immunocompromised, as well as ophthalmic herpes, are emergencies requiring aggressive treatment.

HSV is caused by exposure to a symptomatic or asymptomatic individual infected with HSV-1 or HSV-2, such as a family member, sexual partner, or through occupational contact. Neonatal infection is transmitted via exposure to active lesions during vaginal birth.

• Unprotected sex (ano-genital herpes)
• Medical occupations (e.g., dentists, dental technicians, nurses, and respiratory care unit personnel)
• Vaginal birth (neonatal herpes)
• Wrestling (herpes gladiatorum)
• Compromised immune system

The clinical manifestations and the clinical course depend on the following: anatomic site of the lesions, age at first episode of infection, subtype of the virus, and immune status of the patient. Initial episodes of HSV-1 or HSV-2 can be severe and are often accompanied by systemic signs and symptoms.

• Oral-facial infections—gingivostomatitis (inflammation of the gums and oral mucosa), pharyngitis, fever, facial neuralgia, malaise, myalgias, loss of appetite, irritability, cervical adenopathy, and lesions of the lip, face, gingiva, tongue, and hard and soft palate
• Genital infections—fever, headache, malaise, myalgias, pain, itching, dysuria, vaginal and urethral discharge, inguinal lymphadenopathy, and lesions of the external genitalia, cervix, and urethra. Perianal and anal infections may occur after anal intercourse.
• Neonatal infection (usually disseminated disease)—fever, hypothermia, progressive jaundice, hepatosplenomegaly, vesicular skin lesions, loss of appetite, vomiting, lethargy, respiratory distress, cyanosis, circulatory collapse, and death (if untreated). Neurologic sequelae are common.
• Eye infections (herpes keratitis)—pain, blurred vision, conjunctivitis, edema, corneal lesions, and blindness. (In the United States, HSV is the most common cause of corneal blindness.)
• Infection in immunocompromised persons (usually disseminated disease)—widespread dermal, mucosal, and visceral disease (including pneumonia), long-lasting localized lesions
• Herpetic whitlow (primary or recurrent HSV infection of the finger or hand)—edema, erythema, tenderness, vesicular or pustular lesions, fever, and axillary lymphadenopathy (often from occupational exposure, e.g., dentists)

• Tonsillitis
• Viral encephalitis (or other viral infections)
• Dermatitis
• Vulvovaginitis
• Impetigo
• Conjunctivitis
• Bacterial meningitis
• Bacterial pneumonia

Because HSV has been isolated from many visceral and mucocutaneous sites, there is considerable variability in the clinical manifestations and the course of infection. Primary infections tend to be more severe and of longer duration. Recurrent infections are common because HSV remains latent in the nerve cells of the ganglia or cranial nerve until a trigger causes reactivation after the primary infection.

• Tissue cultures—to show characteristic multinucleated giant cells
• Antigen detection—for group and type discrimination
• Polymerase chain reaction (PCR)—especially for CNS infections
• Serologic assays, especially tissue-specific assays (e.g., complement fixation, passive hemagglutination, indirect immunofluorescence, radioimmunoassay, complement-mediated cytolysis, antibody-dependent cellular cytolysis)—to type isolates

Entry of HSV infection is at mucosal surfaces or breaks in the skin, but disseminated infections may also involve visceral organs and the central nervous system. After the primary infection, HSV infection is maintained by the nerve ganglion cells in a latent state. Reactivation results in the normal pattern of gene expression, replication, and release of HSV. HSV can be shed even if the infection is subclinical.

Magnetic resonance imaging (MRI) and computed tomography (CT)—to locate involved areas of HSV encephalitis

• Electroencephalography (EEG) to locate involved areas of HSV encephalitis.
• Staining of scrapings with Wright, Giemsa, or Papanicolaou stains—to diagnose skin lesions and to view intranuclear inclusions
• Immunoblotting techniques
• Cell-mediated immunity assay

Limited skin lesions can be treated with over-the-counter preparations. Antiviral chemotherapy with acyclovir can successfully treat HSV infections.

Lower dosages of antivirals listed below are for recurrent infections, and higher dosages are for primary infections.

• Intravenous acyclovir (45 to 60 mg/kg/day for 21 days)—for neonatal herpes
• Intravenous acyclovir (10 mg/kg every eight hours for 10 to 14 days)—for HSV encephalitis
• Oral acyclovir (200 to 400 mg three to five times/day)—for mucocutaneous herpes; oral acyclovir (200 to 400 mg tid for 10 days), oral valacyclovir (500 to 1,000 mg bid), and oral famciclovir (125 to 250 mg tid for 5 to 10 days)—for genital lesions
• Oral famciclovir (500 mg bid) and acyclovir (400 mg bid)—to reduce frequency and severity of recurrences
• Ganciclovir—effective against both HSV-1 and HSV-2 but generally too toxic for practical use
• Idoxuridine, trifluridine (one drop 1% solution every two hours), topical vidarabine, acyclovir, and interferon—for herpetic keratitis
• Intravenous foscarnet (40 mg/kg every eight hours for 10 to 24 days)—for acyclovir-resistant HSV

Enhancing the immune system and inhibiting the herpes virus may be achieved through nutritional and herbal support.

• Avoid alcohol, caffeine, refined foods, sugars, saturated fats, and high arginine-containing foods (seeds, grains, nuts, nut butters, and chocolate). Arginine promotes HSV replication.
• Increase intake of high lysine-containing foods (fish, chicken, eggs, potatoes, and dairy products) during active herpes infection. Lysine inhibits HSV replication.
• Vitamin C (1,000 mg tid) and acidophilus (one capsule with meals) may reduce the duration of outbreaks.
• Beta-carotene (50,000 to 100,000 IU/day) inhibits viral activity.
• Zinc (30 mg/day) inhibits viral replication.
• L-lysine (500 to 1,000 mg/day for prevention; 2,000 mg bid to qid during an outbreak) may reduce duration and frequency of outbreaks.
• Thymus extract can help strengthen the immune system.
• Selenium (250 mcg/day) may reduce duration and frequency of outbreaks.
• Vitamin A (200,000 IU/day for 3 days at onset of outbreak) can be helpful to decrease length and severity of symptoms. Contraindicated for pregnant women and those with liver disease.

Herbs are generally a safe way to strengthen and tone the body's systems. As with any therapy, it is important to ascertain a diagnosis before pursuing treatment. Herbs may be used as dried extracts (capsules, powders, teas), glycerites (glycerine extracts), or tinctures (alcohol extracts). Unless otherwise indicated, teas should be made with 1 tsp. herb per cup of hot water. Steep covered 5 to 10 minutes for leaf or flowers, and 10 to 20 minutes for roots. Drink 2 to 4 cups/day. Tinctures may be used singly or in combination as noted.

Topical cream applications of concentrated extracts of lemon balm (Melissa officinalis) and/or glycyrrhizic acid (from licorice root) can provide symptomatic relief and reduce severity and duration of outbreak. They may be applied to both oral and genital lesions. For best results, apply at first sign of outbreak.

Internal treatment supports anti-viral activity and immune function. For acute infection, combine equal parts of the following herbs in a tincture (30 to 60 drops tid to qid) or a tea (3 to 4 cups/day). Coneflower (Echinacea purpurea), licorice root (Glycyrrhiza glabra), lemon balm, yarrow (Achillea millefolium), chamomile (Matricaria recutita), and St. John's wort (Hypericum perforatum). Licorice is contraindicated in hypertension. For recurrent infections, substitute lomatium (Lomatium dissectum) and astragalus (Astragalus membranaceus) for yarrow and chamomile, and use the new formula in tincture form, 30 drops tid. These herbs have a deep-acting, immune-stimulating effect. Lemon balm can be used topically or internally for prevention and treatment of HSV.

An experienced homeopath should assess individual constitutional types and severity of disease to select the correct remedy and potency. For acute prescribing use 3 to 5 pellets of a 12X to 30C remedy every one to four hours until acute symptoms resolve.

• Apis mellifica when lesions are swollen, stinging, and burning; relieved by cold applications.
• Graphites for genital herpes on inner thigh with tremendous itching.
• Petroleum for genital herpes that spread to anus and thighs.

Ice packs applied to oral lesions or to the sacral area for genital lesions may help reduce pain and inflammation. Stress reduction techniques, such as meditation, yoga, or tai chi, improve immune function and help to reduce frequency of outbreaks.

Boosting the immune system, pain relief, and balancing normal physiology are ways in which acupuncture may be helpful.

Therapeutic massage helps to reduce the effects of stress which may exacerbate HSV.

Patients with primary infections must be counseled about infectivity, recurrences, asymptomatic shedding of virus, pregnancy, and sex. Identifying triggers (e.g, ultraviolet light) can help to reduce recurrences if steps are taken to avoid them (e.g, sunscreen). Avoiding contact with infectious lesions (e.g., condoms, gloves) can help prevent primary infections.

Sex should be avoided during outbreaks as condoms do not completely prevent herpes infections. Virus may be transmitted even when no lesions are visible. Cesarean section is advised for pregnant women genitally infected with either HSV-1 or HSV-2 as some recurrences may be asymptomatic. Avoid sunburn or use sunscreen to reduce the risk of recurrent herpes of the lips.

• Herpes keratitis is associated with encephalitis and blindness.
• Genital herpes increases a woman's risk of cervical cancer.
• Infection with herpes at the time of delivery can result in serious, life-threatening infection in the infant.
• A primary infection during pregnancy may result in spontaneous abortion or life-threatening infection in the fetus.
• Oral-facial herpes has been implicated as the etiologic agent in Bell's palsy and erythema multiforme
• Primary infections can be associated with herpes encephalitis and aseptic meningitis.

Most herpes infections resolve without sequelae except for infections in neonates and immunocompromised persons. Frequent recurrences should be expected.

Primary HSV infection in the third trimester of pregnancy can be associated with high mortality and morbidity. Cesarean section is indicated if active genital lesions are present. If an infant becomes infected during delivery, neonatal herpes ensues, often resulting in disseminated infection; neurologic deficits and death are common without antiviral treatment.

Nutritional support is indicated in pregnancy. Topical herbal applications may provide symptomatic relief and decrease duration and severity of outbreaks.

Balch JF, Balch PA. Prescription for Nutritional Healing. 2nd ed. Garden City Park, NY: Avery Publishing; 1997:317-319.

Bartram T. Encyclopedia of Herbal Medicine. Dorset, England: Grace Publishers; 1995:226-227.

Fauci AS, Braunwald E, Isselbacher KJ, et al., eds. Harrison's Principles of Internal Medicine. 14th ed. New York, NY: McGraw-Hill; 1998:1080-1086.

Holmes KK, Mardh PA, Sparling PF. Sexually Transmitted Diseases. 2nd ed. New York, NY: McGraw-Hill; 1995:391-408.

Krugman S, Katz SL, Gershon AA, et al. Infectious Diseases of Children. St. Louis, Mo: Mosby-Year Book; 1992:175-188.

Lad VD. The Complete Book of Ayurvedic Home Remedies. New York, NY: Harmony Books; 1998:200-201.

Mandell GL, Douglas RG Jr, Bennett JE. Principles and Practice of Infectious Diseases. 3rd ed. New York, NY: Churchill Livingstone; 1990:1144-1151.

Milman N, Scheibel J, Jessen O, et al. Lysine prophylaxis in recurrent herpes simplex labialis: a double-blind, controlled crossover study. Acta Derm Venereol. 1980;60:85-87.

Morrison R. Desktop Guide to Keynotes and Confirmatory Symptoms. Albany, Calif: Hahnemann Clinic Publishing; 1993:29, 171, 172, 289.

Murray MT, Pizzorno JE. Encyclopedia of Natural Medicine. 2nd ed. Rocklin, Calif: Prima Publishing; 1998:360, 520-524.

Thein DJ, Hurt WC. Lysine as a prophylactic agent in the treatment of recurrent herpes simplex labialis. Oral Surg Oral Med Oral Pathol. 1984;58:659-666.

Tyler VE. Herbs of Choice: The Therapeutic Use of Phytomedicinals. Binghamton, NY: Pharmaceutical Products Press; 1994:162-166.

Werbach M. Nutritional Influences on Illness. New Canaan, Conn: Keats Publishing; 1988:213-215.