Key role of singlet oxygen and peroxynitrite in viral RNA damage during virucidal effect of plasma torch on feline calicivirus

A dielectric barrier discharge (DBD) plasma torch has been used to evaluate the mechanism underlying inactivation of feline calicivirus (FCV) by plasma treatment. Plasma treatment of cell lysate infected with FCV F9 strain reduced the viral titer of the median tissue culture infectious dose (TCID(50)). The D value (treatment time required to lower the viral titer to 1/10) was 0.450 min, while the viral titer dropped below the detection limit within 2 min. FCV was not significantly inactivated by heat or UV applied at levels corresponding to those generated from the DBD plasma torch after 2 min (38.4 °C and 46.79 mJ/cm(2) UV, respectively). However, TCID(50) was reduced by 2.47 log after exposure to 4.62 mM ONOO(−), corresponding to the concentration generated after 2 min of plasma treatment. Radical scavengers, including superoxide dismutase, dimethyl sulfoxide, and catalase, did not significantly affect viral titers; however, sodium azide, uric acid, and ascorbic acid, which are scavengers of (1)O(2) radicals, ONOO(−), and peroxynitrous acid (ONOOH; produced from ONOO(−) under acidic conditions), respectively, significantly increased TCID(50) and intact viral RNA. These findings suggest that ONOO(−) and (1)O(2) play an important role in FCV inactivation by attacking viral RNA during DBD plasma torch treatment.