AI Article Synopsis

  • Interferon derived from rat fibroblasts (RFA-1) is stable at pH 2 but sensitive to heat and denaturants like SDS and urea, whereas beta-mercaptoethanol does not inactivate it.
  • The yield of interferon production is dependent on the multiplicity of infection (moi) with optimal induction occurring at an moi of 10, and pretreatment with interferon leads to a modest increase in production but faster synthesis.
  • Rat interferon shows significant cross-reactivity, performing effectively on mouse fibroblasts (100-300% activity) but less so on guinea pig, human, and bovine cells (5-10% activity), and it does not induce an antiviral state

Article Abstract

Interferon derived from rat fibroblasts (RFA-1) was pH 2 stable and heat labile. Denaturants such as SDS and urea inactivated this interferon but beta-mercaptoethanol alone did not. IFN yield after Newcastle disease virus was multiplicity of infection (moi) dependent. Optimal induction was obtained with an moi of 10. RFA-1 cells produced small amounts of IFN (less than or equal to 10(1.5) U/ml) when exposed to varying amounts of poly(rI): poly(rC). Addition of DEAE-dextran and/or pretreatment with IFN did not change this response. Pretreatment resulted in increased interferon production, priming, but on the average it was only about a 2-fold increase. However, the kinetics of interferon production were altered by pretreatment with IFN whether there was an increase in production or not. Both IFN synthesis and production peaks were detected 2-4 h earlier in IFN-pretreated RFA-1 cells. Rat IFN exhibited a great deal of cross-species activity. It is 100-300% cross-reactive on mouse (L929B and 3T3) cells, and 5-10% active on guinea pig fibroblasts, human (GM 2767) and bovine (MDBK) cells. These cells were more sensitive to rat IFN than Jensen sarcoma cells (a rat tumour cell line). Neither chicken embryo fibroblasts nor monkey (Vero) cells developed an antiviral state when exposed to rat IFN.

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