DESCRIPTION

Herpes simplex virus (HSV) is an enveloped double-stranded DNA virus. It exists as two distinct subtypes, HSV-1 and HSV-2, and is responsible for a wide spectrum of illness ranging from fever blisters to genital ulcers and fatal encephalitis. It establishes lifelong latency and can lead to interval episodes of asymptomatic shedding and disease recurrence.

EPIDEMIOLOGY

• HSV-1 infects 40–80% of the U.S. population by young adulthood.
• HSV-2 incidence increases during adolescence and adulthood, infecting 20–35% of U.S. adults aged 40 years.
• In the United States, neonatal HSV occurs in approximately 1:2,000 live births every year. The incidence has increased over the last 2 decades.

RISK FACTORS

• Risk factors for HSV-1 and HSV-2 infections include older age and lower socioeconomic status.
• Additional risk factors for HSV-2 include number of lifetime sexual partners and female gender.

GENERAL PREVENTION

• Perinatal infection
  • The majority of neonatal HSV infections (85%) occur through contact with maternal HSV shed within the birth canal. A smaller proportion (5%) of infections occur in utero.
  • The majority (60–80%) of mothers of infected infants have no symptoms of HSV infection at the time of delivery or history of HSV infection.
  • Children born to mothers with primary genital HSV infection at time of delivery are at highest risk (up to 60%). In contrast, the risk of neonatal infection with recurrent maternal genital herpes is significantly lower (2–5%).
  • In the setting of active genital herpes (lesions or pain), cesarean delivery is recommended. However, infections may still occur despite cesarean delivery and intact amniotic membranes.
  • Cesarean delivery is not recommended for mothers with a history of genital HSV in the absence of lesions or symptoms.
  • Fetal scalp monitors should be avoided in women with suspected genital HSV.
  • The use of antiviral therapy (acyclovir or valacyclovir) after 36 weeks’ gestation decreases viral shedding and reactivation of genital lesions in mothers with a history of genital HSV, although breakthrough infections may still occur.
• Postnatal infection (neonates and children)
  • Secretions of active HSV lesions are highly infectious, and asymptomatic viral shedding is common. 10% of neonatal HSV infections are contracted postpartum through direct contact with infectious fluids.
  • Standard universal precautions are appropriate in caring for recurrent/localized lesions in immunocompetent persons.
  • Contact precautions should be considered in neonates, in immunocompromised persons with active lesions, and in severe primary mucocutaneous HSV.
  • Contact with genital/cutaneous HSV lesions (e.g., sexual intercourse, wrestling) should be avoided until lesions resolve.

PATHOPHYSIOLOGY

• Spread occurs typically via contact with abraded skin or mucous membranes.
• The incubation period for primary infection is approximately 2 to 12 days.
• Viral replication begins at the portal of entry (epithelia) and commences within sensory ganglia. Migration occurs back to the site of inoculation, with subsequent destruction of epithelial cells.
• Following initial infection, the virus remains latent in sensory neural ganglia and can be reactivated by UV exposure, trauma, stress, hormonal changes, or immunosuppression.
• HSV antibodies provide a degree of cross protection across serotypes; previous infection with one HSV serotype (e.g., HSV-1) can decrease the severity of infection with the alternate serotype (e.g., HSV-2).
• HSV antiviral resistance is rare among healthy individuals but can develop in immunocompromised hosts and in the setting of herpetic keratitis.

COMMONLY ASSOCIATED CONDITIONS

• Gingivostomatitis
• Encephalitis
• Herpes gladiatorum
• Herpetic whitlow
• Eczema herpeticum
• Erythema multiforme
• Bell palsy