Abstract
Shortly after the discovery of interferon, its broad in vitro antiviral spectrum and potential ability to be applied directly to the upper reratory tract were recognized as desirable characteristics for use in reratory viral infections (1). In 1973 Merigan et al showed that intranasal administration of human leukocyte interferon (HuIFN-α [Le]) in a total dosage of 14 Mu over 4 days reduced seroconversion and illness rates following experimental rhinovirus type 4 challenge (2). A subsequent study at the MRC Conmon Cold Unit by Scott et al utilizing a lower dosage (≥ 0.6 Mu) of fibroblast-derived interferon (IFN-β) found no evidence of protection (3). Scott et al later showed that high dosages of purified IFN-α(Le) (90 Mu over 4 days) protected against experimental rhinovirus type 9-induced illness (4). Studies conducted at Baylor College of Medicine identified rapid nasal clearance and insufficient contact time with the nasal mucosa, concentration dependency of antiviral action, and perhaps inactivation of IFN-β by nasal secretions as factors contributing to the relatively high interferon amounts needed to achieve antiviral effects in the nasal mucosa (5–9).
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© 1988 Kluwer Academic Publishers, Boston
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Hayden, F.G. (1988). Intranasal Interferons for Control of Respiratory Viral Infections. In: Revel, M. (eds) Clinical Aspects of Interferons. Developments in Medical Virology, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1737-1_1
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DOI: https://doi.org/10.1007/978-1-4613-1737-1_1
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