The existence of virus particles with antagonistic activities for interferon induction provides a mechanism for regulating IFN production and the potential outcome of a virus infection.
ISP dominance in coinfected cells may regulate IFN responses; leaves open relevance to infection outcomes in vivo.
Cells generally responded to viral inducers of interferon (IFN) by generating a dose (multiplicity of infection)-response (interferon-yield) curve which showed a good fit to a model in which the fraction of interferon-yielders corresponded to the fraction of cells infected with one or more particles. These were defined as interferon-inducing particles (IFPs). The IFN-producing capacity of cells infected with these particles was modulated upon coinfection with a second type of virus particle, those with the capacity to suppress IFN production. These were termed interferon induction-suppressing particles (ISPs). In cells coinfected with IFP and ISP the latter were dominant phenotypically. In some systems ISP activity was expressed by IFP when the latter were present at two or more particles per cell. The existence of virus particles with antagonistic activities for interferon induction provides a mechanism for regulating the production of IFN and hence the potential outcome of a virus infection.
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Philip I. Marcus (1982) studied this question.
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