Neutralisation of respiratory syncytial virus by cat serum

Abstract

RESPIRATORY SYNCYTIAL (RS) virus has been identified as a major cause of lower respiratory infection in infants, and the epidemiology of RS virus infection is characterised uniquely by annual winter outbreaks in the infant population and by antigenie stability of the virus¹. The initial isolation of RS virus was from a captive chimpanzee² and more recently an antigenically similar virus has been associated with respiratory disease in cattle^3–5. The bovine and human RS viruses, although antigenically similar, can be differentiated by their different host range in vitro⁶. The bovine RS virus had a wider host range, multiplying in bovine, hamster, swine and primate cells, whereas the human RS virus multiplied only in bovine and primate cells. We have observed recently, however, that human RS virus (but not bovine RS virus) can multiply efficiently in secondary cultures of feline embryo cells. The cytopathology induced by RS virus infection of feline embryo cells was similar to that described previously for African green monkey (BS-C-1) cells⁷: the surfaces of infected cells were seen to be covered by long slender filaments when viewed by scanning electron microscopy or by immunofluorescent staining (C.R.P. and J. E. Parry, unpublished data). The susceptibility of feline embryo cells to RS virus, and an observation that the sera of some laboratory cats in the USA inhibited RS virus (R.M. Chanock, personal communication), suggested that cats might be susceptible to RS virus infection. We therefore examined a random sample of cat sera, and we show that antibody to RS virus is widespread in domestic cats in Britain.