Enhancement of IgE-mediated histamine release from human basophils by viruses: role of interferon

The present study showed that incubation of HSV-1, Influenza A, or Adeno-1 viruses with human peripheral blood leukocytes failed to release histamine into the supernatant fluids. If, however, these leukocyte cultures were first incubated with virus and then challenged with ragweed antigen E or anti-IgE, a marked enhancement of histamine release occurred. Both infectious and nonin- fectious viruses were effective. Examination of the culture fluids revealed that the enhancement of histamine release was associated with a soluble factor that had the properties of interferon. Several lines of evidence indicate that interferon, in fact, was responsible for the enhancement of histamine release. First, all stimulants that enhanced histamine release (i.e., viruses and poly I:poly C) also induced interferon. In contrast, stimulants that did not enhance histamine release (Simian foamy virus, PRK cell control, allantoic fluids, RPMI medium) did not induce interferon (25) . Second, there was a direct relationship between both the time of appearance and the amount of interferon in the culture fluids and the degree of histamine enhancement. Third, all preparations of human interferon, regardless of the tissue of origin (i.e. leukocytes or fibroblasts), were effective. Controls not containing interferon and heterologous interferon (i.e. mouse) were ineffective. Fourth, the soluble factor responsible for the enhancement of histamine release could not be dissociated from the antiviral activity of interferon by standard physicochemical means. Whether the enhancement of histamine release by interferon requires new RNA and protein synthesis (e.g., the reputed "antiviral protein" of interferon) is presently under investigation.