Pediatric Herpes Simplex Virus Infection 

  • Author: Swetha G Pinninti, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Jan 24, 2012
 

Background

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[1] 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.[2] 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.

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Pathophysiology

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.[3, 4] 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.[5, 6] Histology of skin lesions shows cellular balloon degeneration, condensation of nuclear chromatin, and formation of multinucleated giant cells.[4]

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.[7] Additionally, titers of antibodies that mediate antibody-dependent cellular cytotoxicity inversely correlate with severity of neonatal infection.[8]

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Epidemiology

Frequency

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).[9, 10]

The seroprevalence rate of HSV-2 in pregnant women ranges from 15-30%.[11] 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%.[12, 13] Overall, approximately 2% of women acquire herpes simplex virus during pregnancy.

International

Herpes simplex virus has worldwide distribution. The prevalence of genital herpes in developing countries is 2-74% and varies among countries.[14, 15] In African countries that are experiencing HIV epidemics, HSV-2 infection is highly prevalent (≥ 70%).[16] 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.[17, 18, 19]

Mortality/Morbidity

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.[2] 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%.[20]

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.[12, 21] 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.[22] Studies determined that herpes simplex virus infection in neonates and infants was associated with substantial morbidity, mortality, and resource use.[23]

Race

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.[24] 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.

Sex

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.[25] 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.

Age

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.[25] 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.[2, 26]

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Contributor Information and Disclosures
Author

Swetha G Pinninti, MD  Fellow in 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, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Coauthor(s)

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Specialty Editor Board

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

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, and Society for Pediatric Research

Disclosure: Medimmune Grant/research funds Cliinical trials; Medimmune Honoraria Speaking and teaching; Medimmune Consulting fee Consulting

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  American Legion 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, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

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, and Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

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

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Primary herpes simplex virus (HSV) gingivostomatitis in an infant is shown. This same patient also had concomitant herpes whitlow as shown in Media file 2.
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.
 
 
 
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