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. 1966 Jan;91(1):251–256. doi: 10.1128/jb.91.1.251-256.1966

Role of Interferon-Like Viral Inhibitor in Endotoxin-Induced Corneal Resistance to Newcastle Disease Virus

J O Oh 1, E J Gill 1
PMCID: PMC315940  PMID: 5948192

Abstract

Oh, J. O. (University of British Columbia, Vancouver, B.C., Canada), and E. J. Gill. Role of interferon-like viral inhibitor in endotoxin-induced corneal resistance to Newcastle disease virus. J. Bacteriol. 91:251–256. 1966.—A state of marked resistance to the toxic corneal effects of Newcastle disease virus (NDV) was observed in rabbit eyes after intravenous injection of 10 or 100 μg of typhoid endotoxin. By use of tissue cultures of rabbit corneal endothelial cells for assay, high titers of an interferon-like viral inhibitor were detected in serum and in ocular aqueous humor of these animals. The pretreatment of eyes with aqueous humor or serum containing the inhibitor markedly suppressed the production of corneal toxicity by NDV. The intravenous injection of 1 μg of the endotoxin had a negligible effect on the corneal reaction, and little or no inhibitor was found in either serum or aqueous humor. Normal aqueous humor or serum contained no inhibitor and had no suppressive effect on the NDV-induced reactions. The results indicated that the inhibitor played an important role in the induction of corneal resistance to NDV in vivo. The inhibitor in aqueous humor of endotoxin-injected rabbits was found to be derived from blood after an increase in the permeability of “blood-aqueous barrier” of iris due to the endotoxin. Therefore, intravenously administered typhoid endotoxin induced corneal resistance to NDV in rabbits through its dual action on host: (i) release of an interferon-like viral inhibitor into the blood stream and (ii) disruption of the blood-aqueous barrier of the iris, thus allowing the passage of the viral inhibitor from blood into the anterior chamber, where it modified the corneal endothelial cells to render them resistant to NDV.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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