Interferon‐Mediated Self‐Limiting Growth of Respiratory Syncytial Virus in Mouse Embryo Cells

Abstract

The growth of respiratory syncytial (RS) virus in primary mouse embryo (ME) cells was investigated. The virus yields in ME cells were markedly lower if compared with those in HEp-2 cells, which are fully permissive for RS virus, and a remarkable production of interferon (IFN) was found in the early period of infection of the former cells. The virus yields in ME cells were enhanced when antimouse IFN serum was added to the medium. Indirect immunofluorescent staining of infected ME cells showed that the infection spread in the entire monolayer in the presence of antiserum, whereas it was markedly restricted throughout in the absence of the serum. All the major viral polypeptides were synthesized in the absence of the serum. However, their synthesis rates were greatly enhanced if the antiserum was added. These results suggest that the virus growth in ME cells is self-limiting and that this limited growth is due to autointerference by endogenously produced IFN during the course of infection. Further, this type of growth restriction of RS virus appears to be characteristic of cells of mouse origin by comparative studies that used other cells of different origin.

Bovine Respiratory Syncytial Virus Nonstructural Proteins NS1 and NS2 Cooperatively Antagonize Alpha/Beta Interferon-Induced Antiviral Response

“…The human counterpart of BRSV, HRSV, was recently reported to be highly resistant to IFNinduced antiviral activity in human cells (2), and it appears that HRSV NS proteins are optimized to antagonize IFN responses of human cells. Adaptation of viral proteins to counteract innate responses in cells of their natural host is an important factor in determining the virus host range and may prevent viruses from crossing species barriers (13,22,26). The V protein of simian virus 5 (SV5) for example, is able to block the activation of IFN-responsive genes in primate cells but not in murine cells (14).…”

“…This is also supported by previous observations. Growth of HRSV in primary mouse embryo cells was markedly restricted; however, when anti-mouse IFN serum was added to the medium, virus yields were enhanced and the infection spread in the entire monolayer (26). In addition, recombinant BRSV in which the G and F surface protein genes were replaced by their HRSV counterparts was somewhat more competent than BRSV for replication in chimpanzees.…”

Analysis of the local and systemic immune responses induced in BALB/c mice by experimental respiratory syncytial virus infection

“…Currently no data other than those presented in the present report have been published on IFN in RS virus infection in vivo using the BALB/c mouse model. However, recent research in vitro has shown that RS virus infection of BALB/c mouse embryo cells as well as C3H mouse-derived L929 cells induces marked IFN production (Hanada et al, 1986). Furthermore, infection of BALB/c mouse embryo cultures was shown to be limited by this response.…”

Respiratory Syncytial Virus (RSV) Nonstructural (NS) Proteins as Host Range Determinants: a Chimeric Bovine RSV with NS Genes from Human RSV Is Attenuated in Interferon-Competent Bovine Cells

“…The contribution of pneumovirus NS proteins to the permissivity of hosts to RSV infection is also supported by other studies. Hanada et al (20) showed that the markedly restricted growth of HRSV in mouse embryo cells could be overcome by adding antimouse IFN serum to the medium. As a result, HRSV yields were enhanced and the infection spread in the entire monolayer.…”