Abstract
Photodynamic inactivation has been known since Raab, at the beginning of the 20th century, observed that acridine was harmless to paramecia in the dark but was lethal when the organisms were exposed to visible light (1). Three decades later viruses were shown to be photosensitive (2, 3). However, assay methods in the 1930s were crude, and no quantitative results were reported. In 1958, Yamamoto (4) reported the first quantitative studies on photodynamic inactivation of bacterial virus; in 1960, Hiatt et al. (5) extended this work to a number of DNA-containing animal viruses, but found that RNA-containing enteroviruses were resistant to photosensitization. We have since learned that naturally photoresistant viruses can be made photosensitive if the virus is grown in cells maintained with medium containing proflavine, neutral red, or acridine orange. During replication of the virus, the photoreactive dye becomes incorporated within the virus structure (6–10). If one looks through the literature, one can see that in most laboratories virus titers could be reduced markedly by “dye-light” treatment, but usually some virus persisted. The point is that, as usually practiced, photoinactivation may not be complete. Transformation by such preparations in which some infectious virus is still present (11) cannot be said to be caused by photoinactivated virus. However, if the procedures described in the papers from our laboratory are carefully followed, photoinactivation can be made total (12–17).
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© 1982 Plenum Press, New York
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Melnick, J.L., Wallis, C. (1982). Photodynamic Inactivation of Herpesvirus. In: Regan, J.D., Parrish, J.A. (eds) The Science of Photomedicine. Photobiology. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-8312-3_19
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DOI: https://doi.org/10.1007/978-1-4684-8312-3_19
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