f Human enteric viruses are among the main causative agents of shellfish-associated outbreaks. In this study, the kinetics of viral bioaccumulation in live oysters and the heat stabilities of the predominant enteric viruses were determined both in tissue culture and in oyster tissues. A human norovirus (HuNoV) GII.4 strain, HuNoV surrogates (murine norovirus [MNV-1], Tulane virus [TV]), hepatitis A virus (HAV), and human rotavirus (RV) bioaccumulated to high titers within oyster tissues, with different patterns of bioaccumulation for the different viruses. We tested the thermal stability of each virus at 62, 72, and 80°C in culture medium. The viruses can be ranked from the most heat resistant to the least stable as follows: HAV, RV, TV, MNV-1. In addition, we found that oyster tissues provided protection to the viruses during heat treatment. To decipher the mechanism underlying viral inactivation by heat, purified TV was treated at 80°C for increasing time intervals. It was found that the integrity of the viral capsid was disrupted, whereas viral genomic RNA remained intact. Interestingly, heat treatment leading to complete loss of TV infectivity was not sufficient to completely disrupt the receptor binding activity of TV, as determined by the porcine gastric mucin-magnetic bead binding assay. Similarly, HuNoV virus-like particles (VLPs) and a HuNoV GII.4 strain retained some receptor binding ability following heat treatment. Although foodborne viruses have variable heat stability, 80°C for >6 min was sufficient to completely inactivate enteric viruses in oysters, with the exception of HAV.A pproximately 7.6 million to 14.5 million illnesses in the United States are attributed to the consumption of contaminated seafood each year, and enteric viruses are responsible for more than 50% of these cases (1). In a review of the available epidemiological evidence, human norovirus (HuNoV) and hepatitis A virus (HAV) were the leading viruses associated with shellfish, accounting for 83.7% and 12.8% of outbreaks, respectively (2). The type of shellfish most frequently associated with viral outbreaks was oysters, which were the vehicle in 58.4% of outbreaks (2). In some regions, human enteric viruses are practically ubiquitous in harvested shellfish. Keller et al. (3) showed that 100% of shellfish samples collected from Vitória Bay, Espírito Santo, Brazil, were positive for rotavirus (RV) and adenovirus. However, only 80% of the growing water samples were positive for these pathogens. Viral titers were 400 times higher in the shellfish samples than in the growing water, indicating high levels of natural bioaccumulation (3). In the Galician Rias area, the largest shellfish production area in the European Union, 55% of mussel, clam, and cockle samples were contaminated by HuNoV genogroup I (GI) and GII and HAV (4). Thus, understanding of the ecology and persistence of enteric viruses in shellfish is needed to help prevent future outbreaks.The consumption of uncooked contaminated bivalve shellfish continues to pose a public ...

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Enteric viruses are shed in fecal material by humans and other animals and are common contaminants in wastewater and surface water. Wastewater treatment plants often disinfect this effluent with low-pressure and medium-pressure UV lamps, which emit 254-nm and 220- to 280-nm irradiation, respectively. It is not known whether this treatment is efficacious against enteric viruses or how such treatments may inactivate these enteric viruses. This study examined UV disinfection for two enteric viruses: rotavirus (RV) (strain OSU with double-stranded RNA and a three-layer capsid) and Tulane virus (TV) (a cultivable surrogate for human norovirus with single-stranded RNA and a single-layer capsid). Viruses were treated with UV irradiation at 220 or 254 nm under conditions relevant to wastewater stabilization ponds, whose water is often used for irrigation. TV was susceptible to 220- or 254-nm UV at similar levels. It appears that UV irradiation inactivated TV by mutagenizing both its genome and capsid binding proteins. RV was more susceptible to UV at 220 nm than to UV at 254 nm. UV irradiation of RV at either 220 or 254 nm resulted in a virus that retained its ability to bind to its host cell receptor. After 220-nm treatment, the VP7 segment of the RV genome could not be amplified by PCR, suggesting that this treatment mutagenized the viral genome. However, this correlation was not observed when UV at 254 nm was used. Thus, RV and TV, with different genome and capsid contents, are targeted by UV irradiation in different ways. IMPORTANCE UV irradiation is becoming common for disinfection in water treatment plants, but little is known about the effectiveness of this treatment for enteric RNA viruses. Here, we observed that 220-nm UV irradiation was efficacious against rotavirus (RV) and Tulane virus (TV). UV irradiation at 254 nm inactivated TV to a greater extent than RV. Additional assays showed that UV irradiation compromised different portions of the RV and TV life cycles. UV irradiation decreased the binding of TV to its host receptor and mutagenized the TV genome. UV irradiation at 220 nm appeared to allow RV–host receptor interaction but halted RV genome replication. These findings provide knowledge about the disinfection of waterborne viruses, information that is important for the safe reuse or release of treated wastewater.

A pandemic such as COVID-19 can cause a sudden depletion of the worldwide supply of respirators, forcing healthcare providers to reuse them. In this study, we systematically evaluated dry heat treatment as a viable option for the safe decontamination of N95 respirators (1860, 3M) before their reuse. We found that the dry heat generated by an electric cooker (100 °C, 5% relative humidity, 50 min) effectively inactivated Tulane virus (TV, >5.2-log 10 reduction), rotavirus (RV, >6.6-log 10 reduction), adenovirus (AdV, >4.0-log 10 reduction), and transmissible gastroenteritis virus (TGEV, >4.7-log 10 reduction). The respirator integrity (determined on the basis of the particle filtration efficiency and quantitative fit testing) was not compromised after 20 cycles of a 50 min dry heat treatment. On the basis of these results, dry heat decontamination generated by an electric cooker (e.g., rice cookers, instant pots, and ovens) could be an effective and accessible decontamination method for the safe reuse of N95 respirators. We recommend users measure the temperature during decontamination to ensure the respirator temperature can be maintained at 100 °C for 50 min.

Two rotavirus (RV) strains (sialidase-resistant Wa and sialidase-sensitive OSU) were irradiated with simulated solar UVA and visible light in sensitizer-free phosphate buffered solution (PBS) (lacking exogenous reactive oxygen species (ROS)) or secondary effluent wastewater (producing ROS). Although light attenuated for up to 15% through the secondary effluent wastewater (SEW), the inactivation efficacies increased by 0.7 log for Wa and 2 log for OSU compared to those in sensitizer-free phosphate buffered solution (PBS) after 4 h of irradiation. A binding assay using magnetic beads coated with porcine gastric mucin containing receptors for rotaviruses (PGM-MB) was developed to determine if inactivation influenced RV binding to its receptors. The linear correlation between the reduction in infectivity and the reduction in binding after irradiation in sensitizer-free solution suggests that the main mechanism of RV inactivation in the absence of exogenous ROS was due to damage to VP8*, the RV protein that binds to host cell receptors. For a given reduction in infectivity, greater damage in VP8* was observed with sialidase-resistant Wa compared to sialidase-sensitive OSU. The lack of correlation between the reduction in infectivity and the reduction in binding, in SEW, led us to include RNase treatment before the binding step to quantify virions with intact protein capsids and exclude virions that can bind to the receptors but have their capsid permeable after irradiation. This assay showed a linear correlation between the reduction in RV infectivity and RV-receptor interactions, suggesting that RV inactivation in SEW was due to compromised capsid proteins other than the VP8* protein. Thus, rotavirus inactivation by UVA and visible light irradiation depends on both the formation of ROS and the stability of viral proteins.

To fill the knowledge gap on how effective free chlorine is against viral-contaminated produce, we inoculated the surfaces of outdoor- or greenhouse-grown kale and mustard with Rotavirus (RV) or a human norovirus surrogate (Tulane virus, TV) and then disinfected the leaves with free chlorine. Disinfection efficacies for RV strain OSU and Wa were approximately 1-log10 higher when attached to mustard than to kale. Similar disinfection efficacies were observed for TV attached to mustard or kale. When examining TV and RV OSU in suspension (not attached to leaf surfaces), TV was more resistant to free chlorine than RV OSU. Inactivation efficacies were higher for these viruses in suspension versus viruses attached to produce the surface. We also found that free chlorine damaged viral capsids, allowing free chlorine access to viral RNA to damage viral genomes. Exposure to free chlorine at 1.7 ppm over 1 min caused VP8* of RV OSU to lose its ability to bind to its host receptors. TV lost its ability to bind to its receptor only after exposure to free chlorine at 29 ppm over 1 min. Thus, to reduce foodborne viral infections, it is important to consider the differences in virus’ reactivity and inactivation mechanisms with free chlorine.

<div> <div> <p>A pandemic such as COVID-19 can cause a sudden depletion in the worldwide supply of respirators, forcing healthcare providers to reuse them. In this study, we systematically evaluated dry heat treatment as a viable option for the safe decontamination of N95 respirators (1860, 3M) before its reuse. We found that the dry heat generated by an electric cooker (100°C, 5% relative humidity, 50 min) effectively inactivated Tulane virus (>5.2-log₁₀ reduction), rotavirus (>6.6-log₁₀ reduction), adenovirus (>4.0-log₁₀ reduction), and transmissible gastroenteritis virus (>4.7-log₁₀ reduction). The respirator integrity (determined based on the particle filtration efficiency and quantitative fit testing) was not compromised after 20 cycles of 50-min dry heat treatment. Based on these results, we propose dry heat decontamination generated by an electric cooker (e.g., rice cookers, instant pots, ovens) to be an effective and accessible decontamination method for the safe reuse of N95 respirators.<br></p> </div> </div>

c Rotavirus (RV) is the major etiological agent of acute gastroenteritis in infants worldwide. Although high-pressure processing (HPP) is a popular method to inactivate enteric pathogens in food, the sensitivity of different virus strains within same species and serotype to HPP is variable. This study aimed to compare the barosensitivities of seven RV strains derived from four serotypes (serotype G1, strains Wa, Ku, and K8; serotype G2, strain S2; serotype G3, strains SA-11 and YO; and serotype G4, strain ST3) following high-pressure treatment. RV strains showed various responses to HPP based on the initial temperature and had different inactivation profiles. Ku, K8, S2, SA-11, YO, and ST3 showed enhanced inactivation at 4°C compared to 20°C. In contrast, strain Wa was not significantly impacted by the initial treatment temperature. Within serotype G1, strain Wa was significantly (P < 0.05) more resistant to HPP than strains Ku and K8. Overall, the resistance of the human RV strains to HPP at 4°C can be ranked as Wa > Ku ‫؍‬ K8 > S2 > YO > ST3, and in terms of serotype the ranking is G1 > G2 > G3 > G4. In addition, pressure treatment of 400 MPa for 2 min was sufficient to eliminate the Wa strain, the most pressure-resistant RV, from oyster tissues. HPP disrupted virion structure but did not degrade viral protein or RNA, providing insight into the mechanism of viral inactivation by HPP. In conclusion, HPP is capable of inactivating RV at commercially acceptable pressures, and the efficacy of inactivation is strain dependent. R otavirus (RV) is the major etiological agent of acute gastroenteritis in infants worldwide (1, 2). RVs are estimated to cause nearly 500,000 deaths annually among children (3, 4). The virus is transmitted by the fecal-oral route, and contaminated water and food are common vehicles for infections (1,5,6). RV belongs to the genus Rotavirus, subfamily Sedoreovirinae, and family Reoviridae. There are eight species (groups) of rotavirus, referred to as A, B, C, D, E, F, G, and H. Humans are infected primarily by species A, B, and C, most commonly by species A. Rotavirus species A can be further divided into different serotypes. RV is a segmented double-stranded RNA virus with a triple-layer icosahedral capsid. The outer capsid glycoprotein (VP7) and the spike protein (VP4) differentiate RVs into 14 G (glycoprotein) serotypes and 27 different P (protease sensitivity) genotypes (1, 3, 4). Currently, five serotypes (G1 to G4 and G9) are the predominant circulating viruses, accounting for almost 95% of strains worldwide (1). Recently, commercial RV vaccines have been used in children to provide immunity against the most commonly circulating strains (4). Despite major efforts, RV outbreaks still occur worldwide due to the high genetic diversity of RVs and lack of cross-protection (2, 7-9). Therefore, alternative strategies for the prevention of RV infection must be established.Enteric viruses are a leading cause of foodborne illnesses. Within foodborne viruses, human norovirus (NoV), rotaviruses (RVs...