Strains of Respiratory Syncytial Virus: Implications for Vaccine Development

Abstract

Within a few years after its discovery in 1957, respiratory syncytial virus (RSV) was shown to be the single most important pathogen of acute lower respiratory tract illness among infants and young children worldwide. In the 1960’s and 1970’s multiple attempts to develop a vaccine failed. The first vaccine was formalin-inactivated, alum precipitated virus grown in primary monkey kidney cells that was evaluated in four field trials (Chin et al. 1969; Fulginiti et al. 1969; Kapikian et al. 1969; Kim et al. 1969). The vaccine induced a good serologic response to RSV but failed to protect the vaccinee from infection and, vaccinees <2 yrs old experienced more severe RSV disease than those not vaccinated. This increase in serious disease is illustrated in Table 1 for one of the trials. Live virus vaccines also failed (Belshe et al. 1982; McKay et al. 1988; Tyeryar, 1983; Wright et al. 1976, 1982). Some vaccine strains reverted to wild phenotype virus during clinical trials and others failed to induce an adequate antibody response. These failures have led researchers to conclude that a better understanding of the virus and the virus host interaction is needed to increase the chances of successfully developing an RSV vaccine.