important for vaccine development. There are two major surface glycoproteins. Neither of them has hemagglutinating or neuraminidase activity; however, one of them is probably responsible for fusion of the viral membrane to infected cells and for fusion of an infected cell to neighboring cells (Walsh and Hruska, 1983). This protein, in an unreduced state, has a molecular weight of 66,000–68,000 (Bernstein and Hruska, 1981).
Monoclonal antibody that immunoprecipitates this protein neutralizes the virus in vitro, prevents formation of syncytia, and may have some protective effect when administered passively to small animals subsequently inoculated with RSV. The other surface glycoprotein has a molecular weight of 84,000–90,000 and has no known function. Monoclonal antibody to this larger glycoprotein may be neutralizing in the presence of complement. Neither of the glycoproteins has yet been purified.
DNA complementary to the RSV genome has been cloned (Collins and Wertz, 1983; Venkatesan et al., 1983), and which of the cloned fragments correspond to the messages for the two surface glycoproteins has been investigated (Collins and Wertz, 1985). The genes coding for the major glycoprotein and fusion protein have apparently now been cloned (National Institute of Allergy and Infectious Diseases, 1985).
RSV infection and disease occur in the very young in the presence of maternal IgG, but there is some evidence that infants with high levels of serum antibody are less often infected or severely ill than infants with low levels (Glezen et al., 1981; Parrot et al., 1973). There is also evidence that partial immunity may be conferred by natural infection; adults who have been inoculated with tissue culture grown virus have shown subsequent resistance to reinfection by the same route (Mills et al., 1971).
Most studies suggest, however, that RSV infection recurs at yearly or biennial intervals under natural conditions (Beem, 1967; Henderson et al., 1979). Reinfections are frequently less severe than first infections, but this appears to be a function of increasing age more than immunity (Henderson et al., 1979). Reinfections in the same RSV epidemic probably are rare, however. It seems likely that secretory immunity is more important in protection against reinfection than systemic immunity, although this point cannot be made with certainty.
The presence of respiratory syncytial viruses as respiratory pathogens is quite uniform worldwide, but the severity and characteristics of disease caused by RSV probably vary. The age of initial acquisition also may vary, although antibody prevalence studies do not show any clear-cut differences between developed and developing countries.