Abstract

Acridine orange-sensitized photoinactivation of tobacco mosaic virus and tobacco mosaic virus-ribonucleic acid has been studied in detail. The intact virus is only partially inactivated by acridine orange even at 10 −5 M acridine orange. Tobacco mosaic virus-ribonucleic acid inactivation by acridine orange has been studied from the standpoint of the ribonucleic acid-dye complexes (Complex I and Complex II), and the ternary complex of ribonucleic acid-dye and metal ions (Complex III). Tobacco mosaic virus-ribonucleic acid infectivity was destroyed with first-order kinetics by low levels of acridine orange (Complex II). “Complex III”, formed in the presence of paramagnetic metal ions, was resistant to photodynamic inactivation, the protection by metal ions being linear with respect to concentration of the metal ions. A comparison of the photosensitization by methylene blue and acridine orange with respect to tobacco mosaic virus-ribonucleic acid and free guanosine showed that, while acridine orange was only 5–6 times less active than methylene blue with ribonucleic acid, it was considerably less efficient in destroying guanosine. Sedimentation studies with acridine orange-inactivated tobacco mosaic virus-ribonucleic acid showed that mild conditions leading to measurable loss of infectivity involve no depolymerization of tobacco mosaic virus-ribonucleic acid which sets in only under more severe conditions. The results have been discussed from the standpoint of the mechanisms of photodynamic inactivation.

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