RSV belongs to the Paramyxoviridae family within the genus Pneumovirus. This genus contains the morphologically and biologically similar pneumonia virus of mice, bovine RSV, ovine RSV, caprine RSV, turkey rhinotracheitis virus, and the recently discovered human metapneumovirus. RSV is an enveloped, medium-sized RNA virus with a nonsegmented, single-stranded, negative-sense genome. Three of the proteins (N, P, and L) are associated with the nucleocapsid, and five (F, G, SH, M, and M2) are associated with the envelope. Two proteins, NS1 and NS2, are nonstructural proteins of the virion. The two major surface glycosylated proteins, F and G, project from the surface, giving the envelope a thistle-like appearance. These glycoproteins appear to be of prime importance in the infectivity and pathogenesis of the virus.

RSV is a notably liable virus, poorly withstanding changes in temperature and pH. RSV in the secretions of patients may survive at room temperature on nonporous surfaces, such as countertops and furniture, for 3 to 30 hours depending on the
humidity. On hands, RSV remains infectious for approximately 0.5 to 1 hour.

Two major strain groups, A and B, with subtypes within each group, have been identified through monoclonal antibody and genomic analyses. The major antigenic variations between these strain groups have been associated primarily with the G protein. Both group A and B strains usually circulate concurrently in a given community. The epidemiologic and clinical importance of infection caused by strains from group A versus group B remains unclear.

RSV infection occurs globally, being identified in every geographic area studied. In most communities, RSV’s seasonal pattern is singular, predictably producing a sizable outbreak of infections each year, especially in temperate climates. In the United States, RSV activity usually lasts for approximately 20 weeks, from November to May, with the peak period of circulation usually occurring during January through March.

The concurrent rise in bronchiolitis and lower respiratory tract illnesses in young children signals an RSV outbreak, even without laboratory confirmation. RSV spreads so effectively among the young that virtually all children have been infected within their first 2 to 3 years of life. During the first year of exposure to RSV, 50% or more of infants acquire infection, and 40% of these infections have been estimated to result in lower respiratory tract illness. Prospective studies of families in Houston showed that 69% of infants acquired RSV infection, and one-third of them had lower respiratory tract disease. In their second year, 83% of children became infected, and 16% had lower respiratory tract disease. Repetitive infections occurred frequently; one-third to one-half of these patients became reinfected in their third and fourth year. The risk of developing an infection is even greater for children in day-care centers, with 65% to 98% acquiring infection during each of their first 3 years.

Infection severe enough to cause hospitalization occurs primarily in infants younger than 12 months of age, especially in those younger than 6 months of age. Recent data from the Centers for Disease Control and Prevention (CDC) have indicated that the annual rates of hospitalization for bronchiolitis increased 2.4 times between 1980 and 1996. RSV was estimated to cause 51,000 to 82,000 bronchiolitis admissions yearly.

The risk factors associated with more severe disease include not only young age but also underlying cardiac or pulmonary disease and host factors of genetic susceptibility associated with specific gene polymorphisms. Other factors that have been associated with augmenting the chance of young children acquiring RSV disease include crowding, lower socioeconomic income, multiple siblings, older school-age siblings, and exposure to passive smoke.

RSV is acquired through the inoculation of respiratory secretions of infected individuals into the nose or eyes of another individual. Close contact with such individuals may result in inoculation from large-particle aerosols generated by sneezing or coughing or by contacting infectious secretions on fomites, with subsequent self-inoculation. After an incubation period of 3 to 6 days, the virus spreads during primary infection along the epithelium of the respiratory tract, producing bronchiolitis and/or pneumonia.

Early in the course of bronchiolitis, a lymphocytic peribronchiolar infiltration associated with edema of the walls and surrounding tissue is evident. Progression of the infection causes the characteristic necrosis and sloughing of the bronchiolar epithelium, resulting in the plugging of the infant’s airways, which are particularly prone because of their small diameter. Impedance to the flow of air occurs during both inspiration and expiration, but it is augmented during expiration when the lumen is narrowed further by the positive expiratory pressure. Air trapped peripheral to the sites of partial occlusion results in the clinical manifestation of hyperinflation of the lung. When complete obstruction occurs, the trapped air may become absorbed, resulting in multiple areas of atelectasis. Lower respiratory tract involvement from RSV commonly exhibits pathologic findings of both bronchiolitis and pneumonia, with interstitial infiltration of mononuclear cells and alveolar filling. Recovery is marked by evidence of regeneration at the bronchiolar epithelium, usually within the first week, but the presence of ciliated cells and complete recovery may require weeks.