Medscape is available in 5 Language Editions – Choose your Edition here.


Pediatric Herpes Simplex Virus Infection

  • Author: Swetha G Pinninti, MD; Chief Editor: Russell W Steele, MD  more...
Updated: Jul 20, 2015

Practice Essentials

Herpes simplex virus (HSV) infections are ubiquitous and have a wide range of clinical manifestations (see the images below). Beyond the neonatal period, most primary HSV-1 infections occur in infancy and childhood and are transmitted primarily by contact with infected saliva. Primary HSV-2 infections are acquired after onset of sexual activity, and genital herpes infections are among the most common sexually transmitted infections.

Primary herpes simplex virus (HSV) gingivostomatit Primary herpes simplex virus (HSV) gingivostomatitis in an infant is shown. This same patient also had concomitant herpes whitlow as shown in the following image.
Herpes whitlow in an infant. Herpes whitlow in an infant.

See 13 Common-to-Rare Infant Skin Conditions, a Critical Images slideshow, to help identify rashes, birthmarks, and other skin conditions encountered in infants.

Also, see the Herpes Simplex Viruses: Test Your Knowledge slideshow for more information on clinical, histologic, and radiographic imaging findings in HSV-1 and HSV-2.

Essential update: AAP clinical practice guidelines

In January 2013, the American Academy of Pediatrics issued new guidelines for the evaluation of asymptomatic neonates exposed to HSV during delivery.[1, 2, 3] The guidelines assume laboratory access to polymerase chain reaction (PCR) assays for HSV DNA or type-specific serologic tests and may not be applicable in clinical settings without rapid testing turnaround times. Recommendations include the following:

  • Women in labor with visible genital lesions should be swabbed for HSV PCR and culture, and positive test results should be further analyzed to distinguish HSV-1 from HSV-2
  • A history of genital herpes should be obtained before the pregnancy
  • In women with a recurrent maternal herpes outbreak, skin and mucosal specimens should be obtained from the neonate for culture and PCR assay about 24 hours after delivery, and blood should be sent for HSV DNA PCR assay; preemptive treatment with acyclovir need not be started if the infant remains asymptomatic; if results become positive within 5 days, confirming neonatal HSV infection, the infant should undergo a complete evaluation to determine the extent of disease, and intravenous acyclovir should be initiated as soon as possible
  • In women without a history of genital herpes who have genital lesions at delivery, serologic testing should be done on maternal samples swabbed during delivery to determine the type of infection present; the infant should undergo a complete evaluation, and IV acyclovir should be initiated; if the mother has a first-episode infection and the neonate’s results are normal, the infant should be treated with IV acyclovir for 10 days; if the neonate’s results are positive, the infant should be treated with IV acyclovir for 14-21 days (depending on the extent of disease) and reevaluated to ensure clearance of the virus; after completion of IV acyclovir treatment, infants should receive suppressive therapy with oral acyclovir for 6 months

Signs and symptoms

HSV causes myriad clinical presentations, as follows:

  • Orolabial infection
  • Genital infection
  • Intrauterine and perinatal infection (herpes neonatorum)
  • Central nervous system infection
  • Infection in immunocompromised hosts
  • Other infections: Herpetic whitlow, herpes gladiatorum, keratoconjunctivitis, Mollaret meningitis, erythema multiforme

Clinical features of orolabial HSV infection include the following[4] :

  • Abrupt onset of illness
  • Fever
  • Listlessness or irritability
  • Inability to eat and/or drink
  • Gingivitis (with markedly swollen, erythematous, and occasionally bleeding gums)
  • Increased drooling in infants due to pain on swallowing
  • Vesicular lesions on the tongue, buccal mucosa, and palate with extension, at times, to the lips and face (these may rupture and coalesce to form large, ulcerated areas)
  • Tender submandibular or cervical adenopathy
  • In recurrent cases, a prodrome of pain, burning, tingling, and itching

Clinical features of genital HSV infection may include the following:

  • In first episodes, severe constitutional symptoms (eg, fever, malaise, myalgias [5] )
  • Initial itching and pain, followed by more troublesome signs and symptoms
  • Lesions that evolve from vesicles to pustules to wet ulcers and heal by crusting
  • Painful inguinal lymphadenopathy, dysuria, and vaginal discharge
  • Paresthesias of the legs and perineum
  • Urinary retention

Herpes neonatorum may be categorized as follows[6, 7, 8, 9, 10] :

  • Skin, eye, and mucous membrane (SEM) disease
  • Disseminated infection
  • CNS infection

Clinical features of HSV CNS infection may include the following:

  • Insidious or abrupt onset
  • Headache, altered consciousness, and focal neurologic abnormalities at presentation
  • Symptoms of aseptic meningitis (headache, fever, stiff neck, photophobia)
  • Symptoms of autonomic nervous system dysfunction and transverse myelitis (eg, hyperesthesia or anesthesia of the lower back, perineum, or sacral region)

See Clin ical Presentation for more detail.


Measures for diagnosing HSV infection in children include the following:

  • Isolation of the virus in tissue cultures (most common confirmation method)
  • Histologic analysis of scrapings or punch biopsy specimens
  • Cytologic evaluation via a Tzanck preparation
  • Serologic testing (only for determining past HSV exposure)
  • PCR assay (preferred for CNS infection [11, 12, 13] and possibly valuable for disseminated disease)
  • Lumbar puncture and cerebrospinal fluid analysis
  • Immunofluorescent microscopy
  • Brain biopsy
  • Imaging studies: Computed tomography, magnetic resonance imaging

See Workup for more detail.


Specific medical therapy for pediatric HSV infection involves antiviral medications. Antiviral agents used include the following:

  • Oral acyclovir (most common)
  • Oral famciclovir (a prodrug that is converted to penciclovir)
  • Oral valacyclovir (a prodrug that is converted to acyclovir)
  • IV acyclovir (for encephalitis, neonatal disease, severe infection in immunocompromised patients, occasional cases of severe orolabial or genital disease, [14, 15, 16, 17] , and recurrent genital HSV infections)

Inpatient management is often indicated for pediatric patients with HSV infections. Suggested criteria include the following:

  • Many children with severe HSV gingivostomatitis who are dehydrated
  • Neonates with disseminated or CNS disease
  • Older patients with encephalitis who may be very ill at presentation
  • HSV infection in immunocompromised patients

Measures to prevent or minimize transmission of genital HSV infection include the following:

  • Avoid contact with individuals excreting the virus (difficult, because they are often asymptomatic)
  • Start oral antiviral therapy at the first symptom or sign of genital HSV disease
  • Promote condom use
  • Provide appropriate evaluation, counseling, and education

Measures to prevent transmission of HSV to newborns include the following:

  • Reassure women with recurrent disease that risk of neonatal infection is low
  • Perform cesarean delivery if a mother has active lesions during delivery [18]
  • Observe infants delivered vaginally by mothers with active genital herpes; follow up neonates carefully, and immediately institute antiviral therapy if symptoms occur [19]
  • In pregnant women with symptomatic genital herpes, consider antiviral suppressive treatment initiated at 36 weeks’ gestation

See Treatment and Medication for more detail.



Herpes simplex virus (HSV) is a double-stranded, enveloped, DNA virus. Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) belong to the family Herpesviridae, subfamily Alphaherpesvirinae. Following initial infection, the herpes viruses become latent in the sensory neural ganglia (the trigeminal ganglion in HSV-1 infection[20] and the sacral ganglion in HSV-2 infection). Herpes simplex virus infections are ubiquitous and cause a wide range of infections from isolated mucocutaneous lesions to disseminated infection in all age groups. Neonatal herpes simplex virus disease is associated with high morbidity and mortality.[19] Herpes simplex virus infections are among the few non-HIV viral infections amenable to antiviral therapy. Available antiviral chemotherapy can be used to treat infection, shorten the clinical course, and, in certain circumstances, prevent infection with herpes simplex virus.



Infection occurs in a susceptible host following exposure of abraded skin or mucosal surfaces to the virus. After inoculation, the virus travels to the sensory ganglion, where it replicates and establishes latency. Recurrence occurs when the virus subsequently migrates along the peripheral sensory nerve, replicates, and produces a typical local lesion.[21, 22] Lifelong latency and periodic recurrences are hallmarks of herpes simplex virus infection. These reactivations can follow exposure to ultraviolet light, stress, hormonal changes, immunosuppression, and other infection.[23, 24] Histology of skin lesions shows cellular balloon degeneration, condensation of nuclear chromatin, and formation of multinucleated giant cells.[22]

Disseminated infection occurs when the host is unable to control viral replication leading to viremia and multiorgan involvement. It is usually seen in neonates and immunocompromised individuals (and very rarely in immunocompetent hosts). Specific immunologic factors responsible for immunity to herpes simplex virus are not completely understood. Both antibody and cell-mediated immunity influence the severity and frequency of recurrences. Herpes simplex virus is also believed to suppress innate immunity by suppressing the production of interferon-alfa and interferon-beta.[25] Additionally, titers of antibodies that mediate antibody-dependent cellular cytotoxicity inversely correlate with severity of neonatal infection.[26]



United States

Herpes simplex virus infections occur throughout the world, with humans serving as the only reservoir. The infection is acquired by intimate mucocutaneous contact between a susceptible host and a symptomatic or asymptomatic host shedding virus during primary infection or reactivation. Because the infection results in lifelong latency, the prevalence in any population is cumulative.

Beyond the neonatal period, most primary HSV-1 infections occur in infancy and childhood and are transmitted primarily by contact with infected saliva. Primary HSV-2 infections are acquired after onset of sexual activity and genital herpes infections are among the most common sexually transmitted infections (STIs).

The prevalence of herpes simplex virus infections depends on socioeconomic status, age, race, and geographic location. For example, approximately 33% of children from lower socioeconomic populations have serologic evidence of herpes simplex virus disease by age 5 years compared with 20% of middle-class individuals. Greater person-to-person contact in crowded living conditions is believed to account for the role of socioeconomic status in prevalence. The importance of daycare attendance is likely, but not well studied.

In the United States, HSV-2 seroprevalence increases from about 20-30% in patients aged 15-29 years to 35-60% in patients aged 60 years. This change represents a 30% increase compared with data from 1976-1980. Factors that increase the frequency of HSV-2 infection in older adolescents and adults include gender (more women than men), race (more blacks than whites), marital status (more divorced individuals than single or married individuals), and place of residence (more city residents than suburban residents).[27, 28]

The seroprevalence rate of HSV-2 in pregnant women ranges from 15-30%.[29] Approximately 10% of pregnant women who are HSV-2 seronegative have a sexual partner who is HSV-2 seropositive and are, therefore, at risk of contracting a primary HSV-2 infection during pregnancy. Transmission typically results from contact with an asymptomatic sexual partner with a reported risk of acquisition of approximately 10%.[30, 31] Overall, approximately 2% of women acquire herpes simplex virus during pregnancy.


Herpes simplex virus has worldwide distribution. The prevalence of genital herpes in developing countries is 2-74% and varies among countries.[32, 33] In African countries that are experiencing HIV epidemics, HSV-2 infection is highly prevalent (≥70%).[34] Evidence suggests that genital herpes simplex virus infection increases the risk of HIV infection and that persons infected with both viruses are more likely to transmit HIV.[35, 36, 37]



Most cases of infection with either HSV-1 or HSV-2 do not result in serious morbidity. Morbidity and mortality associated with herpes simplex virus are discussed in Complications. Mortality associated with herpes simplex virus is primarily related to perinatal infection, encephalitis, and infection in individuals who are immunocompromised.

At the time of vaginal delivery, the risk of herpes simplex virus transmission from a mother with true primary herpes simplex virus infection to her infant is approximately 50%. Women with primary infections at delivery are 10-30 times more likely than women with a recurrent infection to transmit the virus to their babies.[19] Infants born to mothers with newly acquired infections who do not have primary infections in the presence of preexisting immunity caused by another viral infection (ie, first-episode nonprimary) have a transmission risk of 25-30%.[38]

The neonatal herpes simplex virus infection rate is considered to be less than 2% when the mother has active infection caused by the shedding of herpes simplex virus acquired before pregnancy or during gestation before the onset of labor (recurrent infection). Approximately two thirds of women who acquire genital herpes during pregnancy have no symptoms.[30, 39] Of mothers who deliver an infant with herpes simplex virus infection, 60-80% have no evidence of genital herpes simplex virus infection at the time of delivery and have no history of previous genital infection and have sexual partners with no history. Of babies born to mothers with a primary infection near the time of delivery, 30-50% acquire the infection.

Neonatal herpes simplex virus infection is estimated to occur in approximately 1 per 3000 deliveries in the United States. In 2006, a lower incidence of 9.6 cases per 100,000 births was ascertained.[40] Studies determined that herpes simplex virus infection in neonates and infants was associated with substantial morbidity, mortality, and resource use.[41]


Although the risk of herpes simplex virus infection is not related to race, infection rates in the United States vary with race because of various factors, such as racial and ethnic differences in the prevalence of poverty and low socioeconomic status, access to health care, sexual and health-related behavior, and illicit drug use.

By age 5 years, more than 35% of black children are infected with HSV-1 compared with 18% of white children. Through adolescence, the prevalence of antibodies to HSV-1 in blacks is approximately twice the rate among whites. By age 40 years, HSV-1 seroprevalence is similar among blacks and whites. The prevalence of HSV-2 antibodies among blacks is 3-4 times higher than that among whites.

Seroprevalence among women of childbearing age in the late 1970s was estimated to be 50% for blacks and 20% for whites. By the late 1980s, rates of infection had increased to approximately 60% for blacks and 35% for whites. As shown in 2 nationwide surveys of HSV-2 seroprevalence in the last 2 decades, the cumulative lifetime incidence of HSV-2 reaches 25% in white women, 20% in white men, 80% in black women, and 60% in black men.[42] Studies have indicated that the seroprevalence of HSV-2 among Hispanics ranges from 17-22.3%. Infants born to non-Hispanic white women may be at higher risk of herpes simplex virus infections. This is a result of a greater likelihood that these women are herpes simplex virus seronegative and at risk of acquiring a primary HSV-1 or HSV-2 infection in late pregnancy.


Infection rates with HSV-1 tend to be similar in both genders during early childhood. However, through adolescence, the prevalence of antibodies to HSV-1 is slightly higher among females than among males. Rates of HSV-2 infection are higher in women than in men.[43] Nationwide surveys of HSV-2 seroprevalence over the last 2 decades have demonstrated cumulative lifetime incidences of 25% in white women and 80% in black women. This compares with rates of 20% in white men and 60% in black men.


Beyond the neonatal period, most childhood herpes simplex virus infections are caused by HSV-1. The seroprevalence of HSV-1 antibodies increases with age, and its rate is 20% by age 5 years. No increase occurs until 20-40 years of age, when 40-60% of individuals are HSV-1 seropositive. As a reflection of the association between infection and sexual activity, many HSV-2 infections occur around puberty and early adolescence. A progressive increase in HSV-2 infections occurs in all populations beginning in adolescence.[43] In the United States, HSV-2 seroprevalence increases from approximately 20-30% in those aged 15-29 years to 35-60% in those aged 60 years. Most neonatal infections are caused by HSV-2, but increasing proportions are being caused by HSV-1.[19, 44]

Contributor Information and Disclosures

Swetha G Pinninti, MD Assistant Professor of Pediatric Infectious Diseases, Department of Pediatrics, University of Alabama at Birmingham School of Medicine

Swetha G Pinninti, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Mark R Schleiss, MD Minnesota American Legion and Auxiliary Heart Research Foundation Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Medical School

Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Leonard R Krilov, MD Chief of Pediatric Infectious Diseases and International Adoption, Vice Chair, Department of Pediatrics, Winthrop University Hospital; Professor of Pediatrics, Stony Brook University School of Medicine

Leonard R Krilov, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Pediatric Research

Disclosure: Nothing to disclose.


The authors and editors of Medscape Drugs & Diseases gratefully acknowledge the contributions of previous author Sherman Alter, MD, to the original writing and development of this article.

  1. Hede K. New guidelines for neonates exposed to HSV during delivery. Medscape Medical News. Jan 28, 2013. Available at Accessed: Feb 5, 2013.

  2. [Guideline] Kimberlin DW, Baley J; Committee on Infectious Diseases; Committee on Fetus and Newborn. Guidance on management of asymptomatic neonates born to women with active genital herpes lesions. Pediatrics. 2013 Feb;131(2):383-6:[Full Text].

  3. Kimberlin DW, Baley J. Guidance on management of asymptomatic neonates born to women with active genital herpes lesions. Pediatrics. 2013 Feb. 131(2):e635-46. [Medline]. [Full Text].

  4. Arduino PG, Porter SR. Herpes Simplex Virus Type 1 infection: overview on relevant clinico-pathological features. J Oral Pathol Med. 2008 Feb. 37(2):107-21. [Medline].

  5. Johnston C, Magaret A, Selke S, Remington M, Corey L, Wald A. Herpes simplex virus viremia during primary genital infection. J Infect Dis. 2008 Jul 1. 198(1):31-4. [Medline].

  6. Kimberlin DW. Herpes simplex virus infections in neonates and early childhood. Semin Pediatr Infect Dis. 2005 Oct. 16(4):271-81. [Medline].

  7. Kimberlin DW. Herpes simplex virus infections of the newborn. Semin Perinatol. 2007 Feb. 31(1):19-25. [Medline].

  8. Kimberlin DW, Whitley RJ. Neonatal herpes: what have we learned. Semin Pediatr Infect Dis. 2005 Jan. 16(1):7-16. [Medline].

  9. Kimberlin D. Herpes simplex virus, meningitis and encephalitis in neonates. Herpes. 2004 Jun. 11 Suppl 2:65A-76A. [Medline].

  10. Jacobs RF. Neonatal herpes simplex virus infections. Semin Perinatol. 1998 Feb. 22(1):64-71. [Medline].

  11. Kimberlin DW, Lakeman FD, Arvin AM, Prober CG, Corey L, Powell DA. Application of the polymerase chain reaction to the diagnosis and management of neonatal herpes simplex virus disease. National Institute of Allergy and Infectious Diseases Collaborative Antiviral Study Group. J Infect Dis. 1996 Dec. 174(6):1162-7. [Medline].

  12. Golden WC. Polymerase chain reaction in neonatal HSV encephalitis: an assay to count on?. J Perinatol. 2009 Apr. 29(4):259-61. [Medline].

  13. Kimberlin DW. Diagnosis of herpes simplex virus in the era of polymerase chain reaction. Pediatr Infect Dis J. 2006 Sep. 25(9):841-2. [Medline].

  14. Herpes Simplex. Pickering LK, Baker CJ, Kimberlin DW, Long SS. Red Book. 28th ed. American academy of Pediatrics; 2009. 363-373.

  15. Jones CA, Walker KS, Badawi N. Antiviral agents for treatment of herpes simplex virus infection in neonates. Cochrane Database Syst Rev. 2009 Jul 8. CD004206. [Medline].

  16. Gardella C, Brown ZA. Managing genital herpes infections in pregnancy. Cleve Clin J Med. 2007 Mar. 74(3):217-24. [Medline].

  17. Kimberlin DW, Lin CY, Jacobs RF, et al. Safety and efficacy of high-dose intravenous acyclovir in the management of neonatal herpes simplex virus infections. Pediatrics. 2001 Aug. 108(2):230-8. [Medline].

  18. Randolph AG, Washington AE, Prober CG. Cesarean delivery for women presenting with genital herpes lesions. Efficacy, risks, and costs. JAMA. 1993 Jul 7. 270(1):77-82. [Medline].

  19. Corey L, Wald A. Maternal and neonatal herpes simplex virus infections. N Engl J Med. 2009 Oct 1. 361(14):1376-85. [Medline]. [Full Text].

  20. Richter ER, Dias JK, Gilbert JE 2nd, Atherton SS. Distribution of herpes simplex virus type 1 and varicella zoster virus in ganglia of the human head and neck. J Infect Dis. 2009 Dec 15. 200(12):1901-6. [Medline]. [Full Text].

  21. Arvin AM, Whitley RJ, Gutierrez KM. Herpes Simplex Virus Infections. Remington JS, Klein JO, Wilson CB, Baker CJ, eds. Infectious Diseases of the Fetus and Newborn Infant. 6th ed. Philadelphia, PA: Elsevier Saunders; 2006. 845-65.

  22. Charles G Prober. Herpes Simplex Virus. Long SS, Pickering LK, Prober CG. Principles and practice of pediatric infectious diseases. 3rd ed. Chuchill Livingston-Saunders; 2008. 1012-1021.

  23. Freeman ML, Sheridan BS, Bonneau RH, Hendricks RL. Psychological stress compromises CD8+ T cell control of latent herpes simplex virus type 1 infections. J Immunol. 2007 Jul 1. 179(1):322-8. [Medline]. [Full Text].

  24. Ichihashi M, Nagai H, Matsunaga K. Sunlight is an important causative factor of recurrent herpes simplex. Cutis. 2004 Nov. 74(5 Suppl):14-8. [Medline].

  25. Peng T, Zhu J, Klock A, et al. Evasion of the mucosal innate immune system by herpes simplex virus type 2. J Virol. 2009 Dec. 83(23):12559-68. [Medline]. [Full Text].

  26. Kohl S. Role of antibody-dependent cellular cytotoxicity in neonatal infection with herpes simplex virus. Rev Infect Dis. 1991 Nov-Dec. 13 Suppl 11:S950-2. [Medline].

  27. Armstrong GL, Schillinger J, Markowitz L, Nahmias AJ, Johnson RE, McQuillan GM. Incidence of herpes simplex virus type 2 infection in the United States. Am J Epidemiol. 2001 May 1. 153(9):912-20. [Medline].

  28. Leone P, Fleming DT, Gilsenan AW, Li L, Justus S. Seroprevalence of herpes simplex virus-2 in suburban primary care offices in the United States. Sex Transm Dis. 2004 May. 31(5):311-6. [Medline].

  29. Xu F, Markowitz LE, Gottlieb SL, Berman SM. Seroprevalence of herpes simplex virus types 1 and 2 in pregnant women in the United States. Am J Obstet Gynecol. 2007 Jan. 196(1):43.e1-6. [Medline].

  30. Brown ZA, Selke S, Zeh J, et al. The acquisition of herpes simplex virus during pregnancy. N Engl J Med. 1997 Aug 21. 337(8):509-15. [Medline].

  31. Gardella C, Brown Z, Wald A, et al. Risk factors for herpes simplex virus transmission to pregnant women: a couples study. Am J Obstet Gynecol. 2005 Dec. 193(6):1891-9. [Medline].

  32. Weiss H. Epidemiology of herpes simplex virus type 2 infection in the developing world. Herpes. 2004 Apr. 11 Suppl 1:24A-35A. [Medline].

  33. Paz-Bailey G, Ramaswamy M, Hawkes SJ, Geretti AM. Herpes simplex virus type 2: epidemiology and management options in developing countries. Sex Transm Infect. 2007 Feb. 83(1):16-22. [Medline]. [Full Text].

  34. Celum C, Levine R, Weaver M, Wald A. Genital herpes and human immunodeficiency virus: double trouble. Bull World Health Organ. 2004 Jun. 82(6):447-53. [Medline]. [Full Text].

  35. Reynolds SJ. Role of HSV-2 suppressive therapy for HIV prevention. Future Microbiol. 2009 Nov. 4:1095-7. [Medline].

  36. Zariffard MR, Saifuddin M, Finnegan A, Spear GT. HSV type 2 infection increases HIV DNA detection in vaginal tissue of mice expressing human CD4 and CCR5. AIDS Res Hum Retroviruses. 2009 Nov. 25(11):1157-64. [Medline]. [Full Text].

  37. Kane CT, Diawara S, Ndiaye HD, et al. Concentrated and linked epidemics of both HSV-2 and HIV-1/HIV-2 infections in Senegal: public health impacts of the spread of HIV. Int J STD AIDS. 2009 Nov. 20(11):793-6. [Medline].

  38. Bernstein DI, Lovett MA, Bryson YJ. Serologic analysis of first-episode nonprimary genital herpes simplex virus infection. Presence of type 2 antibody in acute serum samples. Am J Med. 1984 Dec. 77(6):1055-60. [Medline].

  39. Brown ZA, Gardella C, Wald A, Morrow RA, Corey L. Genital herpes complicating pregnancy. Obstet Gynecol. 2005 Oct. 106(4):845-56. [Medline].

  40. Flagg EW, Weinstock H. Incidence of neonatal herpes simplex virus infections in the United States, 2006. Pediatrics. 2011 Jan. 127(1):e1-8. [Medline].

  41. Ambroggio L, Lorch SA, Mohamad Z, Mossey J, Shah SS. Congenital anomalies and resource utilization in neonates infected with herpes simplex virus. Sex Transm Dis. 2009 Nov. 36(11):680-5. [Medline]. [Full Text].

  42. Armstrong GL, Schillinger J, Markowitz L, Nahmias AJ, Johnson RE, McQuillan GM. Incidence of herpes simplex virus type 2 infection in the United States. Am J Epidemiol. 2001 May 1. 153(9):912-20. [Medline].

  43. Smith JS, Robinson NJ. Age-specific prevalence of infection with herpes simplex virus types 2 and 1: a global review. J Infect Dis. 2002 Oct 15. 186 Suppl 1:S3-28. [Medline].

  44. Dye DW, Simmons GT. Fatal Herpes Virus Type I Infection in a Newborn. Am J Forensic Med Pathol. 2009 Nov 24. [Medline].

  45. Malvy D, Ezzedine K, Lancon F, et al. Epidemiology of orofacial herpes simplex virus infections in the general population in France: results of the HERPIMAX study. J Eur Acad Dermatol Venereol. 2007 Nov. 21(10):1398-403. [Medline].

  46. Wald A, Zeh J, Selke S, Ashley RL, Corey L. Virologic characteristics of subclinical and symptomatic genital herpes infections. N Engl J Med. 1995 Sep 21. 333(12):770-5. [Medline].

  47. Schiffer JT, Corey L. New concepts in understanding genital herpes. Curr Infect Dis Rep. 2009 Nov. 11(6):457-64. [Medline]. [Full Text].

  48. Koch LH, Fisher RG, Chen C, Foster MM, Bass WT, Williams JV. Congenital herpes simplex virus infection: two unique cutaneous presentations associated with probable intrauterine transmission. J Am Acad Dermatol. 2009 Feb. 60(2):312-5. [Medline].

  49. Marquez L, Levy ML, Munoz FM, Palazzi DL. A report of three cases and review of intrauterine herpes simplex virus infection. Pediatr Infect Dis J. 2011 Feb. 30(2):153-7. [Medline].

  50. Johnson RT. Acute encephalitis. Clin Infect Dis. 1996 Aug. 23(2):219-224; quiz 225-6. [Medline].

  51. Whitley RJ, Gnann JW. Viral encephalitis: familiar infections and emerging pathogens. Lancet. 2002 Feb 9. 359(9305):507-13. [Medline].

  52. Whitley RJ, Kimberlin DW. Viral encephalitis. Pediatr Rev. 1999 Jun. 20(6):192-8. [Medline].

  53. Herget GW, Riede UN, Schmitt-Graff A, et al. Generalized herpes simplex virus infection in an immunocompromised patient--report of a case and review of the literature. Pathol Res Pract. 2005. 201(2):123-9. [Medline].

  54. Simoons-Smit AM, Kraan EM, Beishuizen A, Strack van Schijndel RJ, Vandenbroucke-Grauls CM. Herpes simplex virus type 1 and respiratory disease in critically-ill patients: Real pathogen or innocent bystander?. Clin Microbiol Infect. 2006 Nov. 12(11):1050-9. [Medline].

  55. Wu IB, Schwartz RA. Herpetic whitlow. Cutis. 2007 Mar. 79(3):193-6. [Medline].

  56. Anderson BJ. The epidemiology and clinical analysis of several outbreaks of herpes gladiatorum. Med Sci Sports Exerc. 2003 Nov. 35(11):1809-14. [Medline].

  57. Souza PM, Holland EJ, Huang AJ. Bilateral herpetic keratoconjunctivitis. Ophthalmology. 2003 Mar. 110(3):493-6. [Medline].

  58. Dylewski JS, Bekhor S. Mollaret's meningitis caused by herpes simplex virus type 2: case report and literature review. Eur J Clin Microbiol Infect Dis. 2004 Jul. 23(7):560-2. [Medline].

  59. Ayangco L, Sheridan PJ, Rogers RS. Erythema multiforme secondary to herpes simplex infection: a case report. J Periodontol. 2001 Jul. 72(7):953-7. [Medline].

  60. Whitley RJ. Herpes Simplex Virus in Children. Curr Treat Options Neurol. 2002 May. 4(3):231-237. [Medline].

  61. Sen P, Barton SE. Genital herpes and its management. BMJ. 2007 May 19. 334(7602):1048-52. [Medline].

  62. Melvin AJ, Mohan KM, Schiffer JT, Drolette LM, Magaret A, Corey L, et al. Plasma and cerebrospinal fluid herpes simplex virus levels at diagnosis and outcome of neonatal infection. J Pediatr. 2015 Apr. 166 (4):827-33. [Medline].

  63. Gaensbauer JT, Birkholz M, Pfannenstein K, Todd JK. Herpes PCR testing and empiric acyclovir use beyond the neonatal period. Pediatrics. 2014 Sep. 134(3):e651-6. [Medline].

  64. Shah SS, Aronson PL, Mohamad Z, Lorch SA. Delayed acyclovir therapy and death among neonates with herpes simplex virus infection. Pediatrics. 2011 Dec. 128(6):1153-60. [Medline].

  65. Corey L, Wald A, Patel R, et al. Once-daily valacyclovir to reduce the risk of transmission of genital herpes. N Engl J Med. 2004 Jan 1. 350(1):11-20. [Medline].

  66. Wald A. New therapies and prevention strategies for genital herpes. Clin Infect Dis. 1999 Jan. 28 Suppl 1:S4-13. [Medline].

  67. [Guideline] ACOG Practice Bulletin. Clinical management guidelines for obstetrician-gynecologists. No. 82 June 2007. Management of herpes in pregnancy. Obstet Gynecol. 2007 Jun. 109(6):1489-98. [Medline].

  68. Money D, Steben M,. Guidelines for the management of herpes simplex virus in pregnancy. J Obstet Gynaecol Can. 2008 Jun. 30(6):514-26. [Medline].

  69. Baker DA. Consequences of herpes simplex virus in pregnancy and their prevention. Curr Opin Infect Dis. 2007 Feb. 20(1):73-6. [Medline].

  70. [Guideline] U.S. Preventive Services Task Force (USPSTF). Screening for genital herpes: Recommendation statement. Agency for Healthcare Research and Quality (AHRQ). 2005.

  71. Pinninti SG, Angara R, Feja KN, Kimberlin DW, Leach CT, Conrad DA, et al. Neonatal Herpes Disease following Maternal Antenatal Antiviral Suppressive Therapy: A Multicenter Case Series. J Pediatr. 2012 Feb 14. [Medline].

  72. Kimberlin D, Powell D, Gruber W, et al. Administration of oral acyclovir suppressive therapy after neonatal herpes simplex virus disease limited to the skin, eyes and mouth: results of a phase I/II trial. Pediatr Infect Dis J. 1996 Mar. 15(3):247-54. [Medline].

  73. Kimberlin DW, Whitley RJ, Wan W, et al. Oral acyclovir suppression and neurodevelopment after neonatal herpes. N Engl J Med. 2011 Oct 6. 365(14):1284-92. [Medline].

  74. Martin ET, Krantz E, Gottlieb SL, Magaret AS, Langenberg A, Stanberry L. A pooled analysis of the effect of condoms in preventing HSV-2 acquisition. Arch Intern Med. 2009 Jul 13. 169(13):1233-40. [Medline]. [Full Text].

  75. Pasternak B, Hviid A. Use of acyclovir, valacyclovir, and famciclovir in the first trimester of pregnancy and the risk of birth defects. JAMA. 2010 Aug 25. 304(8):859-66. [Medline].

  76. Mills JL, Carter TC. Acyclovir exposure and birth defects: an important advance, but more are needed. JAMA. 2010 Aug 25. 304(8):905-6. [Medline].

  77. Jaiyeoba O, Amaya MI, Soper DE, Kilby JM. Preventing neonatal transmission of herpes simplex virus. Clin Obstet Gynecol. 2012 Jun. 55(2):510-20. [Medline].

  78. Robinson JL, Vaudry WL, Forgie SE, Lee BE. Prevention, recognition and management of neonatal HSV infections. Expert Rev Anti Infect Ther. 2012 Jun. 10(6):675-85. [Medline].

  79. Straface G, Selmin A, Zanardo V, De Santis M, Ercoli A, Scambia G. Herpes simplex virus infection in pregnancy. Infect Dis Obstet Gynecol. 2012. 2012:385697. [Medline]. [Full Text].

Primary herpes simplex virus (HSV) gingivostomatitis in an infant is shown. This same patient also had concomitant herpes whitlow as shown in the following image.
Herpes whitlow in an infant.
Cutaneous herpes simplex virus (HSV) lesions in a child in whom sexual abuse is suspected.
Vesicular scalp lesions caused by herpes simplex virus (HSV) in a 7-day-old infant.
Herpes gladiatorum in an adolescent wrestler.
MRI shows abnormal signal intensity in the left temporal lobe of an 18-year-old man with herpes simplex virus (HSV) encephalitis.
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.