Several models (animal caliciviruses, poliovirus 1 [PV1], and F-specific RNA bacteriophages) are usually used to predict inactivation of nonculturable viruses. For the same UV fluence, viral inactivation observed in the literature varies from 0 to 5 logs according to the models and the methods (infectivity versus molecular biology). The lack of knowledge concerning the mechanisms of inactivation due to UV prevents us from selecting the best model. In this context, determining if viral genome degradation may explain the loss of infectivity under UV radiation becomes essential. Thus, four virus models (PV1 and three F-specific RNA phages: MS2, GA, and Q␤) were exposed to UV radiation from 0 to 150 mJ · cm ؊2 . PV1 is the least-resistant virus, while MS2 and GA phages are the most resistant, with phage Q␤ having an intermediate sensitivity; respectively, 6-log, 2.3-log, 2.5-log, and 4-log decreases for 50 mJ · cm ؊2 . In parallel, analysis of RNA degradation demonstrated that this phenomenon depends on the fragment size for PV1 as well as for MS2. Long fragments (above 2,000 bases) for PV1 and MS2 fell rapidly to the background level (>1.3-log decrease) for 20 mJ · cm ؊2 and 60 mJ · cm ؊ 2 , respectively. Nevertheless, the size of the viral RNA is not the only factor affecting UV-induced RNA degradation, since viral RNA was more rapidly degraded in PV1 than in the MS2 phage with a similar size. Finally, extrapolation of inactivation and UV-induced RNA degradation kinetics highlights that genome degradation could fully explain UV-induced viral inactivation.Noroviruses, including the RNA genome, are nonculturable viruses of major concern for the safety of drinking water because they are an important cause of waterborne disease (14). Therefore, viral models should be used to estimate their loss of infectivity due to UV radiation. Depending upon the model virus (animal caliciviruses, enteric viruses such as poliovirus 1 [PV1], or RNA phages such as the MS2 phage) and the methods (infectivity versus molecular biology), the UV inactivation of human noroviruses can be estimated between 0 and 5 logs for a 20-mJ · cmϪ 2 fluence (1,5,6,12,21,25,34,35). Moreover, if only one model, such as animal caliciviruses, is considered, UV inactivation studies describe a 1.5-to 5-log unit decline for 20 mJ · cmϪ 2 for both feline and canine caliciviruses (5,6,25,34). Data obtained from these studies show a high variability for the UV susceptibility of viruses. The diversity of the proposed methods also highlights the lack of knowledge concerning the effect of UV on viral particles. Clear data will have to come forward defining the main parameter (i.e., genome size or capsid structure) responsible for viral inactivation before one or another approach can be favored.Although UV inactivates viruses by altering their genome or capsid, most inactivation studies have focused attention on the influence of radiation on DNA rather than on RNA genomes. Specific targets of UV have been demonstrated among the bases constituting the viral genome. In...

Aims:  This study was undertaken to gain an understanding of the factors that influence viral RNA degradation in the presence of chlorine dioxide (ClO2), which will be very useful in helping to define the significance of the presence of the viral genome in disinfected water. Methods and Results:  We focused our investigation on the influence of ClO2 on extracted RNA on the one hand, and on the infectious virus on the other. Our first results show that RNA degradation, like viral inactivation, is dose dependent. The influence of the spatial organization of the targeted genomic sequence, as well as that of its size and location (and/or sequence) on degradation of the Poliovirus 1 genome by ClO2, was studied using real‐time reverse transcriptase‐polymerase chain reaction (RT‐PCR). The results show that the preferential sites of action of ClO2 appear to be located in the untranslated regions, 5′‐ and 3′‐UTR, a phenomenon influenced by both the presence of secondary structures and the genomic sequence in these regions. Our results also reveal a rapid decrease of infectious particles quantified by the cell culture for the applied dose. Comparison between cell culture and real‐time PCR for viral detection reveals disagreement following disinfection treatment, even for the largest targeted fragment (a 6989‐base fragment representing the quasi‐whole viral genome). Conclusions:  The detection of genome fragments is insufficient to confirm the presence of the infectious virus, as each targeted fragment shows a different sensitivity. Hence, the smallest targeted fragment (76 bp) persisted throughout the analysis period, while the longest targeted fragment (6989 bp) disappeared very rapidly. Highly sensitive regions (i.e. 5′‐ and 3′‐UTR) should be targeted to avoid an overestimation of the risk of viral infection using molecular biology methods in water following disinfection. Further studies in this area are needed. Significance and Impact of the Study:  To date, it has not been possible to routinely apply virological controls to drinking water because of the time‐consuming nature of the gold standard technique (cell culture) and its inability to detect all serotypes (e.g. Norovirus). Molecular techniques (e.g. real‐time RT‐PCR) constitute a solution to the rapid and specific detection of all the serotypes. However, ignorance of the mechanisms of viral degradation prevents the validation of PCR for the measurement of the risk of infection to humans following disinfection treatment.