Respiratory Syncytial Virus (See Also: Bronchiolitis)



  • An enveloped, nonsegmented RNA virus of the family Paramyxoviridae and in the subfamily Pneumovirinae along with human metapneumovirus. There are two subgroups, A and B, differentiated by the major attachment G protein, a large surface glycoprotein. The fusion or F protein is relatively homologous between the two subgroups.
  • It is the most common cause of bronchiolitis, a lower respiratory tract disease that primarily affects the small airways.


  • Incubation period is 2 to 8 days.
  • Virus is detected in secretions 4 days prior to clinical symptoms. Typically shedding of infectious virions is 3 to 8 days but can be as long as 3 to 4 weeks in immunocompromised.
  • Transmission occurs by direct contact of nasopharyngeal or ocular mucosa with infected secretions or fomites.
  • Nosocomial spread can occur because the virus can survive on surfaces for several hours and hands for 30 minutes or more.
  • In the United States, epidemics typically occur between November and April and last for roughly 18 to 20 weeks.
  • In tropical climates, respiratory syncytial virus (RSV) seasons are less predictable and can circulate year-round.
  • One antigenic strain predominates during any given epidemic, but both subtypes can circulate concurrently.


  • Peak incidence is the first 2 years of life, and 20–30% of infected infants develop lower respiratory tract disease.
  • Annual rate of RSV-associated hospitalization is roughly 3/1,000 in children <5 years of age and 17/1,000 in children <6 months of age.


  • 50% of children are infected by their first birthday. 100% of children are infected by age of 2 years.
  • Reinfection can occur during the same RSV season and is common during the first few years of life.
  • Subsequent infections are typically milder.

Risk Factors

Those at greatest risk for severe infection include:

  • Children <1 year of age, especially those <6 months of age
  • Children born prematurely (<35 weeks’ gestation)
  • Children with underlying cardiopulmonary disease (e.g., chronic lung disease of prematurity, congenital heart disease)
  • Those with primary immune deficits
  • Patients on immunosuppressive medications (e.g., transplant patients, oncology patients)

General Prevention

  • There is currently no RSV vaccine. A formalin-inactivated RSV vaccine tested in the 1960s caused enhanced illness after reexposure to wild-type RSV likely due to an overexuberant immune response.
  • Because RSV can survive on surfaces, strict hand washing can minimize nosocomial spread.
  • Contact isolation with routine usage of gowns and gloves has been shown to decrease RSV nosocomial spread.
  • Patients with RSV infection should be isolated in private rooms or cohorted.
  • Palivizumab, a humanized monoclonal antibody directed against the highly conserved F protein of RSV, is the only product available for the prevention of RSV infection in certain high-risk children.
    • Children who should receive palivizumab:
      • Infants born before 29 weeks’ gestation
      • Preterm infants with chronic lung disease of prematurity. In these children, palivizumab should also be given during the 2nd year of life if they are receiving medical therapy (e.g., oxygen, chronic corticosteroids, or diuretics) for chronic lung disease.
    • Children for whom palivizumab should be considered:
      • Infants with hemodynamically significant congenital heart disease, anatomic pulmonary abnormalities, or neuromuscular disease
      • Children <24 months who will be profoundly immunocompromised during RSV season
    • Palivizumab is given IM (15 mg/kg) every 30 days for a maximum of 5 doses during RSV season (usually from October/November to March/April).
    • Palivizumab prophylaxis should be discontinued if a patient experiences a breakthrough RSV hospitalization due to the low likelihood of another RSV hospitalization in the same season.
    • Specific recommendations (last updated in 2014) are available from the American Academy of Pediatrics (AAP).


  • The G protein is the major surface glycoprotein responsible for attachment of virus to cells.
  • The F protein aids in viral entry in to cells and is responsible for fusion of adjacent cells to form a syncytia.
  • Infection is initiated in nasopharynx and then can move to the lower respiratory tract.
  • Infection of smaller airways leads to edema and necrosis of epithelial cells and infiltration of inflammatory cells, resulting in airway obstruction and air trapping.
  • Severe RSV infection has been associated with recurrent wheezing later in life. It is unclear whether RSV infection causes subsequent wheezing or if patients predisposed to severe wheezing are more likely to have severe RSV disease.

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