The 40–80 nt region in the 5′‐NCR of genome is a critical target for inactivating poliovirus by chlorine dioxide

Abstract

Chemical disinfection is the most common method used to inactivate viruses from drinking water throughout the world. In this study, cell culture, ELISA, RT-PCR, and spot hybridization were employed to investigate the mechanism underlying chlorine dioxide (ClO(2) )-induced inactivation of Poliovirus type 1 (PV1), which was also confirmed by recombinant viral genome RNA infection models. The results suggested that ClO(2) inactivated PV1 primarily by disrupting the 5'-non-coding region (5'-NCR) of the PV1 genome. Further study revealed that ClO(2) degraded specifically the 40-80 nucleotides (nt) region in the 5'-NCR. Recombinant viral genome RNA infection models confirmed that PV1 RNA lacking this 40-80 nt region was not infectious. This study not only elucidated the mechanism of PV1 inactivation by ClO(2), but also defined the critical genetic target for the disinfectant to inactivate Poliovirus. This study also provides a strategy by which rapid, accurate, and molecular methods based on sensitive genetic targets may be established for evaluating the effects of disinfectants on viruses.

Host-virus interaction: the antiviral defense function of small interfering RNAs can be enhanced by host microRNA-7 in vitro

“…However, siRNAs that targeted the 5′-UTR of picornavirus failed to reduce virus replication29, whereas Pelletier et al found that a combination of two synthetic siRNAs targeting both the 5′-UTR and the 3D polymerase of PV was more effective and persistent than a single siRNA6. Additionally, in our previous study, we found that the PV 5′-UTR was a critical region for its disinfection by chlorine dioxide30. Interestingly, in the present study, we found that a specific siRNA, targeting the region between nucleotides 100–125 of the PV 5′-UTR strongly inhibited viroplasm formation in the context of PV infection and blocked PV-induced cell killing in virally infected Vero and A549 cells.…”

“…The 5′-UTR has six stem-loop domains, representing two functional elements: (1) Domain I is the 1–80 nt region that forms a cloverleaf structure and is associated with the replication of viral nucleic acids. (2) Domains II–VI, in the 130–610 nt region, are associated with the synthesis of viral proteins6253031. In view of the fact that the specific siRNA-100 target sequence is located between nucleotides 100–125, which itself falls between Domains I and II, we hypothesized that this may help to prevent the stem-loop secondary structures from shielding the viral target RNAs access to the RNAi machinery.…”

“…Poliovirus type 1 strain LSc 2ab used in the study was titrated by the 50% tissue culture infectious dose (TCID 50 ) method as previously described30.…”

Inactivation Kinetics and Mechanism of a Human Norovirus Surrogate on Stainless Steel Coupons via Chlorine Dioxide Gas

“…It has been suggested that the inactivation mechanism of hepatitis A virus (a picornavirus) by ClO 2 was due to the loss of the 5= untranslated region of the genome and/or receptor-binding domain destruction on the capsid (53). It was also found that ClO 2 inactivated poliovirus, another picornavirus, primarily by disrupting a 40-to 80-nucleotide sequence in the 5=-noncoding region of the genome (54). On the other hand, working with bacteriophage MS2, it was found that the primary inactivation action of ClO 2 is viral protein degradation, not damage to the viral genome (55).…”

Comparison of the virucidal efficacy of peracetic acid, potassium monopersulphate and sodium hypochlorite on bacteriophages P001 and MS2

“…Genome alterations can also be induced. Some authors have suggested for chlorine dioxide that certain areas of the genome are more sensitive than others and are degraded differently (Simonet and Gantzer 2006;Jin et al 2012). These mechanisms could partially explain the underestimation induced by RT-qPCR approaches targeting short genome sequences compared to infectivity tests on bacteria or cell cultures for determining the inactivation of bacteriophages or viruses after exposure to disinfectants Park et al 2014).…”