Herpes simplex virus primes mouse macrophages for a genetically determined respiratory burst mediated in an autocrine manner by interferon (IFN)-α/β. We have analysed the effect of IFN-α/β on the respiratory burst capacity of mouse peritoneal macrophages by luminol-dependent chemiluminescence using phorbol myristate acetate as trigger. Crude macrophage-produced IFN-α/β as well as purified IFN-α and -β regularly augmented the respiratory burst capacity of peritoneal cells in a concentration-dependent manner. The augmented response was exclusively mediated by macrophages and was manifest after 4 h incubation with IFN-α/β, peaked after 8 h and gradually declined to near background levels after 24 h. The effect of macrophage-produced IFN-α/β was completely abolished by preincubation of IFN with antiserum to IFN-α/β. The data obtained with this antiserum indicated that endogenous IFN, undetectable by a standard cytopathic effect-inhibition assay, was sometimes spontaneously produced by the peritoneal cells. Furthermore, the crude macrophage preparation seemed to contain a macrophage deactivating factor counteracting the effect of IFN-α/β. Genetic analysis of the sensitivity of macrophages for the respiratory burst-priming effect of IFN-α/β revealed that the trait is inherited as a co-dominant autosomal feature. Macrophages from herpes simplex virus-resistant C57BL/6 mice were more sensitive than macrophages from virus-susceptible BALB/c mice and cells from mice of the reciprocal crosses showed an equal sensitivity intermediate between those of the parental strains. A physiological role of differential IFN sensitivity in the context of resistance to virus infections is suggested.


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