Norovirus Infection

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Complicated norovirus infection and assessment of severity by a modified Vesikari disease score system in hospitalized children

Complicated norovirus infection and assessment of severity by a modified Vesikari disease score system in hospitalized children

During the period from 2004 to 2012, there were 957 hospitalized pediatric patients fulfilled study criteria ini- tially enrolled. After the exclusion of 11 with bacterial infection, 7 finally diagnosed as specific disease other than infections, and 19 with incomplete clinical data col- lection, a total of 920 pediatric patients were finally en- rolled. Among them, 207 (22.5 %) were positive for NoV in their fecal samples by RT-PCR method and 189 after excluding 18 with mixed infections, including 10 with rotavirus, 3 with astrovirus, 2 with enteric adenovirus, 1 with sapovirus, 1 with rotavirus and astrovirus, and 1 with Salmonella. The age distridution of the 920 en- rolled children was 18 day- 247 months old (Mean: 31.6 months, median: 24 months), and of norovirus in- fection was 1–240 months old (mean 26.7 months, me- dian: 17 months). Norovirus infection was confirmed in patients admitted in the four major outbreaks of 2004/ 2005 winter, 2006/2007 winter, 2008/09/10 winter, and 2011/2012 winter in 35 (11.6 %), 75 (41.4 %), 36 (15.9 %), and 43 (20.5 %) patients, respectively.

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Epidemiology and clinical features of rotavirus and norovirus infection among children in Ji’nan, China

Epidemiology and clinical features of rotavirus and norovirus infection among children in Ji’nan, China

In this study, we detected typical symptoms for rotavirus and norovirus infections including diarrhea, vomiting and fever. Among patients with rotavirus infection, vomiting was more common than fever and watery stool, which was similar to the results from children with norovirus infection. Rotavirus infections resulted in a higher rate of vomiting and fever than that of norovirus infection. However, the presence of watery stool was at a similar level. Comparison of the frequency of diarrhea and vomiting and the degree of fever between rotavirus and norovirus infections, there was no significant difference to find. Among 80 patients with norovirus infection, 54 (67.5%) had vomiting and 37(46.3%) had fever, which was consistent with a previous study in China [25]. However, the rates of vomiting and fever from a survey carried out in adults in Beijing were 27.1% and 2.1% respectively, which were lower than that from our study. These findings indicated that norovirus infection resulted in a higher rate of vomiting and fever in children than in adults.

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Title: Status of knowledge, attitudes, and practices regarding norovirus infection and

Title: Status of knowledge, attitudes, and practices regarding norovirus infection and

This study aimed to understand the status of knowledge, attitudes, and practices (KAP) of norovirus infection among primary and junior middle school students in Chizhou City, explore its influencing factors. A multistage stratified random sampling method was used to randomly select 1200 students from 8 primary and junior middle schools for the effective questionnaire survey in Chizhou City. A multivariate logistic regression analysis was used to analyse the possible influencing factors. Of 1176 participants, the average knowledge score of norovirus infection was (9.8 ± 3.6), and the scoring rate was 65.3%. The average attitude score was (11.6 ± 1.2), and the scoring rate was 96.3%. The average practice score was (10.4 ± 1.5), and the scoring rate was 86.9%. The difference in the average scoring rate among the three was statistically significant (P < 0.001). The four independent variables of county, education level, sex and age group statistically correlated with the knowledge score. Primary and junior middle school students in Chizhou City had a good attitude and practice compliance in the prevention and control of norovirus infection; however, their professional knowledge still needed further improvement.

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Risk factors for symptomatic and asymptomatic norovirus infection in the community

Risk factors for symptomatic and asymptomatic norovirus infection in the community

We investigated exposures which are recognized to be associated with norovirus-associated IID, or which may be involved in these transmission routes. A hierarchical conceptual framework [19] was used to investigate risk factors, separately, for norovirus- associated IID and asymptomatic norovirus infection (Table 1 ; Supplementary File 3 provides published references to support the conceptual framework). The conceptual framework had three levels : (i) distal fac- tors, which are general characteristics and long-term behaviours, e.g. socioeconomic and demographic in- formation ; (ii) intermediate factors, which are specific behaviours that may increase the risk of exposure for a short time but are not necessarily always a direct source of infection ; and (iii) proximal factors which are a direct source of infection. Reporting of inter- mediate and proximal risk factors was limited to the previous 10 days before symptom onset for norovirus cases, and the 10 days before questionnaire com- pletion for asymptomatic norovirus infections and norovirus negative controls.

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Using Molecular Epidemiology To Trace Transmission of Nosocomial Norovirus Infection

Using Molecular Epidemiology To Trace Transmission of Nosocomial Norovirus Infection

Statistical analysis. To test for differences in proportions of nosocomial in- fection, the following steps were taken. First, the proportion of nosocomial cases within all cases (based on the cutoff of onset of norovirus illness ⬎ 4 days after admission) was calculated for the genotype categories GII.4, GII.7, GII.3, re- maining genotypes, and unknown. These were calculated separately for young children (0 to 5 years) and the remainder of patients (⬎5 years), as young children are potentially at increased risk for norovirus infection and therefore virus introduction into a hospital is more common for this age group. In these calculations, we excluded patients who had been diagnosed between 2 and 4 days after hospitalization, as the distinction between hospital-acquired and commu- nity-acquired infection was not always possible (n ⫽ 44). Second, using the chi-square test of independence, we tested whether the proportion of nosocomial infection was independent of (i) genotype, within each age group; (ii) age, within each genotype; (iii) genotype, within all ages; and (iv) age, within all genotypes. Because we were testing multiple hypotheses (nine in total), we needed to adjust the chi-square P values to control for false discoveries. We used the Benjamini- Hochberg method, as this method has more power than other Bonferroni-type procedures (2). A relationship was considered significant if the adjusted P value did not exceed 0.05.

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The Effect of Malnutrition on Norovirus Infection

The Effect of Malnutrition on Norovirus Infection

ABSTRACT Human noroviruses are the primary cause of severe childhood diarrhea in the United States, and they are of particular clinical importance in pediatric populations in the developing world. A major contributing factor to the general increased sever- ity of infectious diseases in these regions is malnutrition—nutritional status shapes host immune responses and the composi- tion of the host intestinal microbiota, both of which can influence the outcome of pathogenic infections. In terms of enteric no- rovirus infections, mucosal immunity and intestinal microbes are likely to contribute to the infection outcome in substantial ways. We probed these interactions using a murine model of malnutrition and murine norovirus infection. Our results reveal that malnutrition is associated with more severe norovirus infections as defined by weight loss, impaired control of norovirus infections, reduced antiviral antibody responses, loss of protective immunity, and enhanced viral evolution. Moreover, the mi- crobiota is dramatically altered by malnutrition. Interestingly, murine norovirus infection also causes changes in the host micro- bial composition within the intestine but only in healthy mice. In fact, the infection-associated microbiota resembles the malnutrition-associated microbiota. Collectively, these findings represent an extensive characterization of a new malnutrition model of norovirus infection that will ultimately facilitate elucidation of the nutritionally regulated host parameters that predis- pose to more severe infections and impaired memory immune responses. In a broad sense, this model may provide insight into the reduced efficacy of oral vaccines in malnourished hosts and the potential for malnourished individuals to act as reservoirs of emergent virus strains.

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Infection of Calves with Bovine Norovirus GIII.1 Strain Jena Virus: an Experimental Model To Study the Pathogenesis of Norovirus Infection

Infection of Calves with Bovine Norovirus GIII.1 Strain Jena Virus: an Experimental Model To Study the Pathogenesis of Norovirus Infection

The experimental infection of newborn calves with bovine norovirus was used as a homologous large animal model to study the pathogenesis of norovirus infection and to determine target cells for viral replication. Six newborn calves were inoculated orally with Jena virus (JV), a bovine norovirus GIII.1 strain, and six calves served as mock-inoculated controls. Following infection, calves were euthanized before the onset of diarrhea (12 h postinoculation [hpi]), shortly after the onset of diarrhea (18 to 21 hpi), and postconvalescence (4 days pi [dpi]). Calves inoculated with JV developed severe watery diarrhea at 14 to 16 hpi, and this symptom lasted for 53.5 to 67.0 h. Intestinal lesions were characterized by severe villus atrophy together with loss and attenuation of villus epithelium. Viral capsid antigen (JV antigen) was detected by immunohistochemistry in the cytoplasm of epithelial cells on villi. In addition, granular material positive for JV antigen was detected in the lamina propria of villi. Lesions first appeared at 12 hpi and were most extensive at 18 to 19 hpi, extending from midjejunum to ileum. The intestinal mucosa had completely recovered at 4 dpi. There was no indication of systemic infection as described for norovirus infection in mice. JV was found in intestinal contents by reverse transcription-PCR (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) as early as 12 hpi. Fecal shedding of the virus started at 13 hpi and stopped at 23 hpi or at necropsy (4 dpi), respectively. Throughout the trial, none of the control calves tested positive for JV by ELISA or RT-PCR.

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Murine norovirus infection does not cause major disruptions in the murine intestinal microbiota

Murine norovirus infection does not cause major disruptions in the murine intestinal microbiota

This study used two separate but complementary experi- mental designs to examine the response of the murine in- testinal microbiota to MNV infection. The first study addressed the impact of MNV infection on tissue- associated bacterial communities in Swiss Webster mice, while the second study examined fecal bacterial communi- ties in C57BL/6 mice. Results from both experiments demonstrated that the microbial communities in intestinal tissue or feces of Swiss Webster or C57BL/6 mouse strains did not exhibit major alterations following MNV infection. This was true even for the distal ileum, the site of highest MNV-1 replication [16], indicating that viral replication in intestinal tissues of wild-type mice does not lead to major, local disruptions of the microbiota. In analogy, a recent study demonstrated that MNV titers also are not predictive of intestinal pathology in wild-type mice [35]. Furthermore, no large-scale changes in the intestinal microbiota were seen in the setting of three different MNV strains, includ- ing CR6 and MNV-4. These strains were hypothesized to cause disruptions in the microbiota because they were previously implicated in phenotypic alterations of IBD, a disease linked to the dysbiosis of the intestinal micro- biome, and caused a Crohn’s-like disease in a microbiota- dependent manner [20,21]. One major difference between the studies is that the disease phenotypes were observed in genetically altered mouse strains, while the current study was performed in wild-type mice. Since mouse genotype is known to influence the make-up of the bacterial commu- nity in the intestine [36], future studies are needed to ad- dress whether mouse genotype determines the ability of MNV infection to alter the intestinal microbiota.

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Oral Norovirus Infection Is Blocked in Mice Lacking Peyer's Patches and Mature M Cells

Oral Norovirus Infection Is Blocked in Mice Lacking Peyer's Patches and Mature M Cells

A critical early step in murine norovirus (MNV) pathogenesis is crossing the intestinal epithelial barrier to reach the target cells for replication, i.e., macrophages, dendritic cells, and B cells. Our previous work showed that MNV replication decreases in the intestines of mice conditionally depleted of microfold (M) cells. To define the importance of Peyer’s patch (PP) M cells during MNV pathogenesis, we used a model of BALB/c mice deficient in recombination-activating gene 2 (Rag2) and the common gamma chain ( ␥ c) (Rag- ␥ c ⴚ/ⴚ ), which lack gut-associated lymphoid tissues (GALT), such as Peyer’s patches, and mature GP2 ⴙ M cells. Rag- ␥ c ⴚ/ⴚ mice were infected intraperitoneally or perorally with MNV-1 or CR3 for 24 or 72 h. Although the intestinal laminae propriae of Rag-␥c ⴚ/ⴚ mice have a higher frequency of certain MNV target cells (dendritic cells and macrophages) than

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Norovirus Infection in Community Children with Acute Gastroenteritis in Savar Area, Dhaka, Bangladesh

Norovirus Infection in Community Children with Acute Gastroenteritis in Savar Area, Dhaka, Bangladesh

Usually rotavirus infection gets more priority than norovirus or other viral gastroenteritis. As such, two commercially available rotavirus vaccines, Rotarix TM and RotaTeq TM , are licensed in Bangladesh and the Government of Bangladesh has decided to include them in the routine vaccination program in coming years. It is postulated that rotavirus infection prevalence will drop after the nationwide implementation of the vaccine. Then, norovirus might take an advantage and become the most common cause of childhood diarrhea in future. Therefore, detailed studies covering epidemiology, clinical features, treatment and preventive strategies of norovirus should be taken into consideration. Although noroviruses are well recognized as a cause of epidemic acute gastroenteritis in adults and older children in developed countries, their role as an endemic diarrheal pathogen in developing countries has still been neglected. Our study rooted the baseline data of the incidence of norovirus infection among children as an important etiologic agent of diarrhea in community level in a region of Bangladesh. The findings necessitate more studies covering other regions to build a study baseline of norovirus complications throughout the country. Considering the impact of gastroenteritis and the real prevalence of these viruses, effective public health measures should be opted to manage and prevent this infection. Continued Surveillance on gastroenteritis patients as well as in asymptomatic controls needs to be continued for further elucidating the exact role and burden of noroviruses in diarrheal diseases.

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Evidence for Human Norovirus Infection of Dogs in the United Kingdom

Evidence for Human Norovirus Infection of Dogs in the United Kingdom

The viral RNA survey conducted as part of this project did not reveal any canine stool samples containing HuNoV RNA. This implies that the incidence of HuNoV shedding by this population of dogs is negligible, despite samples being collected from healthy dogs (117 animals), dogs with nongastroenteric disease (64 ani- mals), and dogs with severe gastroenteritis requiring veterinary attention (67 animals). Inclusion of samples from the latter two groups was essential, as it has been suggested that HuNoV may be more likely to infect dogs with underlying disease or immunode- ficiency (17), and as canine-specific noroviruses are associated with gastroenteritis in dogs (3, 36), it was hypothesized that HuNoV infection of dogs may cause signs of gastroenteric disease. Gastroenteritis is a common condition in dogs, with an owner questionnaire reporting diarrhea in 14.9% of dogs within the pre- vious 2-week period (37) and 6% of canine veterinary consulta- tions addressing gastroenteritis as a primary complaint (38). Of the 67 dogs with gastroenteritis in our survey, CPV (10 dogs) and CECoV (2 dogs) were detected in 17.9%. This proves that while viral gastroenteritis is relatively common in dogs, noroviruses are not a major cause of viral disease in the population of dogs sam- pled. The likelihood of HuNoV infection in a dog resulting in clinical signs of gastroenteritis is clearly much lower than that of CPV and CECoV infection, and as such, there is no immediate cause for concern by owners and veterinarians.

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Evidence for human norovirus infection of dogs in the UK

Evidence for human norovirus infection of dogs in the UK

The viral RNA survey conducted as part of this project did not reveal any canine stool samples containing HuNoV RNA. This implies that the incidence of HuNoV shedding by this population of dogs is negligible, despite samples being collected from healthy dogs (117 animals), dogs with nongastroenteric disease (64 ani- mals), and dogs with severe gastroenteritis requiring veterinary attention (67 animals). Inclusion of samples from the latter two groups was essential, as it has been suggested that HuNoV may be more likely to infect dogs with underlying disease or immunode- ficiency (17), and as canine-specific noroviruses are associated with gastroenteritis in dogs (3, 36), it was hypothesized that HuNoV infection of dogs may cause signs of gastroenteric disease. Gastroenteritis is a common condition in dogs, with an owner questionnaire reporting diarrhea in 14.9% of dogs within the pre- vious 2-week period (37) and 6% of canine veterinary consulta- tions addressing gastroenteritis as a primary complaint (38). Of the 67 dogs with gastroenteritis in our survey, CPV (10 dogs) and CECoV (2 dogs) were detected in 17.9%. This proves that while viral gastroenteritis is relatively common in dogs, noroviruses are not a major cause of viral disease in the population of dogs sam- pled. The likelihood of HuNoV infection in a dog resulting in clinical signs of gastroenteritis is clearly much lower than that of CPV and CECoV infection, and as such, there is no immediate cause for concern by owners and veterinarians.

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Single Base Substitutions in the Capsid Region of the Norovirus Genome during Viral Shedding in Cases of Infection in Areas Where Norovirus Infection Is Endemic

Single Base Substitutions in the Capsid Region of the Norovirus Genome during Viral Shedding in Cases of Infection in Areas Where Norovirus Infection Is Endemic

Norovirus (NoV) infections are the major cause of food- and waterborne nonbacterial gastroenteritis in Japan. Some individuals showed long-term excretion of the virus into feces in 29 outbreaks of acute nonbac- terial gastroenteritis that occurred in Toyama Prefecture, Japan, in fiscal year 2006. In one of these cases, single base substitutions from A to G in the capsid region of the NoV genome were commonly detected in two individuals during virus shedding by direct sequencing of PCR products. The A-to-G substitution was accom- panied by an N-to-S amino acid change. The population of clones that possessed A at the corresponding site was gradually replaced by those with G during the infectious course. Although other substitutions were observed in the complete open reading frame 2 sequence, they were not common in these two individuals. NoVs are capable of evolving in the gastroenteric tract.

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Antibody Is Critical for the Clearance of Murine Norovirus Infection

Antibody Is Critical for the Clearance of Murine Norovirus Infection

Extensive studies have demonstrated that humoral immune responses are generated by challenge with various norovirus strains in humans, pigs, cattle, and mice (5, 10, 13, 22, 23, 27, 37, 39, 44–46). Studies of natural norovirus infections in human populations show that the lowest rates of seroconversion are in the 0- to 5-year-old age group and, by adulthood, seroconver- sion rates range from 80 to 100% in most countries (reviewed in reference 32). Among children ⬍ 5 years old, a higher base- line titer of norovirus antibody appears to correlate with pro- tection from infection; however, in adults, a preexisting titer does not appear to be protective (37). This suggests that in children, antibody may be protective, whereas in adults, sero- positivity may merely be a sign of previous infection. However, a Norwalk virus challenge study that examined the timing of virus-specific immunoglobulin A (IgA) production demon- strated that an elevation in salivary IgA occurred more than 5 days after infection in susceptible individuals, whereas in indi- viduals resistant to infection, IgA levels were elevated earlier, 1 to 5 days postchallenge (28). This suggests a correlation between the timing of an increase in norovirus specific mucosal IgA production and whether virus established a productive infection in the host.

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Cysteine protease activation and apoptosis in Murine norovirus infection

Cysteine protease activation and apoptosis in Murine norovirus infection

much earlier during MNV infection of RAW264.7 cells, or that there is some off target labeling by the probe. The data presented in figure 3, shows that the polycaspase FLICA signal is greater than the sum of the specific probes. The extra signal in this channel could potentially be con- tributed to caspases that were not tested (1, 4, 6, 10, and 13), however, based on the previous FCV and MNV results this seems unlikely. We believe that the extra signal resulted from off-target labeling. This is strongly sup- ported by the positive identification of cathepsin B by affinity purification of proteins labeled during infection. Other groups have suggested that caspase inhibitors are not highly specific and can target other proteases such as cathepsins [41-44]. While off-target labeling is a signifi- cant limitation for traditional uses of such molecules, it is an advantageous property when combined with affinity purification and peptide mass finger printing to identify other active proteases that may play a role in the infection. Regardless of whether the labeling is on or off-target, the enzyme must be catalytically active for covalent modifica- tion to occur. Figure 3 also shows that the more specific caspase probes are not subject to the same cross reactivity and activation of caspase 3; this follows closely with the recently reported data for MNV [29].

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Murine Norovirus: a Model System To Study Norovirus Biology and Pathogenesis

Murine Norovirus: a Model System To Study Norovirus Biology and Pathogenesis

The characteristic clinical manifestations of human norovi- rus infection are projectile vomiting and/or explosive, watery diarrhea, as well as low-grade fever, malaise, nausea, and ab- dominal cramping or pain (23). In addition, a certain propor- tion of human norovirus infections are asymptomatic (22, 60). A murine model cannot recapitulate norovirus-induced vom- iting, since mice lack an emetic reflex. However, other symp- toms of human norovirus infection can be measured. To date, adult 129 and juvenile CD1 mice do not exhibit any clinical symptoms when inoculated with MNV-1 (30, 36). In addition, juvenile CD1 mice do not develop any clinical symptoms when inoculated with three new strains of MNV, namely, MNV2, MNV3, and MNV4 (Hsu et al., submitted). However, these studies have examined only a few murine norovirus isolates and have focused on a limited number of mouse strains. Given the diversity of host responses observed for different mouse strains and the ongoing characterization of new MNV isolates, we have only begun to understand the pathogenic potential of MNV in laboratory mice. Interestingly, only six amino acids differ between wild-type porcine enteric calicivirus-Cowden (PEC-Cowden), a sapovirus, and tissue culture-adapted PEC- Cowden (24). However, wild-type PEC-Cowden causes diar- rhea in gnotobiotic pigs, while tissue culture-adapted PEC- Cowden does not (25). In light of these data, a more thorough investigation using different mouse and virus strains, infection routes, and virus doses is clearly needed to determine the presence or absence of MNV-induced disease in wild-type hosts.

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Emergence of GI.6 Outbreaks in a High School in Fangshan District, Beijing, China

Emergence of GI.6 Outbreaks in a High School in Fangshan District, Beijing, China

An epidemiological investigation was conducted to spot the possible causes. We define a suspected case for a student in this high school with at least three of the following symptoms: vomiting, nausea, diarrhea and abdominal pain, Confirmed cases for those Suspected cases with positive laboratory confirmation of exsistence of the norovirus, and Controls for students or staffs without symptoms of diarrhea and vomiting within the longest incubation period of norovirus infection (72 h) after exposure to suspected risk factors. Demographicclinical data and Questionnaire survey were conducted to investigate the conditions of food and water that the students used. Survey and tested Data were analyzed by Excel, version 2010(Microsoft) and SPSS for Windows, version 18.0 (SPSS Inc, USA). Categorical variables for exposure of students and controls were analyzed by Chi-square or Fisher’s exact test. All comparisons were two tailed and P-value <0.05 was considered significant.

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Multiple norovirus infections in a birth cohort in a Peruvian peri urban community

Multiple norovirus infections in a birth cohort in a Peruvian periurban community

test or Mann-Whitney U test . The same variables were com- pared for the first and second infection within the same child. To evaluate associations between norovirus infection and growth, multiple linear regression models were generated with the outcome length-for-age and weight-for-age z scores (LAZ and WAZ, respectively) [13]. Analyses adjusted for breastfeed- ing prevalence included data only from children with ≥ 6 months of follow-up. To test if the observed frequencies of ge- notypes in repeated infections were signi fi cantly different than expected by chance, we generated a simulation of 1 million children with a mean of 3 norovirus infections randomly dis- tributed according to the genotype prevalence found in the study population. The genotype frequencies expected by chance were compared with the observed frequencies by a 2- sample proportion test for a binomial distribution. Analyses were performed using Stata software, version 12 (StataCorp, College Station, Texas).

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Regulation of Norovirus Virulence by the VP1 Protruding Domain Correlates with B Cell Infection Efficiency

Regulation of Norovirus Virulence by the VP1 Protruding Domain Correlates with B Cell Infection Efficiency

Human noroviruses are a leading cause of gastroenteritis across the globe, but the pathogenic mechanisms responsible for dis- ease are not well established. The availability of a murine norovirus model system provides the opportunity to elucidate viral and host determinants of virulence in a natural host. For example, previous studies have revealed that the protruding domain of the murine norovirus capsid protein VP1, specifically residue 296 of VP1, regulates virulent infection. We identified a panel of non- synonymous mutations in the open reading frame 2 (ORF2) gene encoding VP1 that arose in persistently infected mice and tested whether these mutations conferred phenotypic changes to viral replication and virulence. Consistent with previous stud- ies, we demonstrate that a glutamic acid at position 296 results in attenuation. For the first time, we also demonstrate that a lysine at this position is sufficient to confer virulence on an otherwise attenuated murine norovirus strain. Moreover, our studies reveal a direct correlation between the efficiency of viral replication in B cells and virulence. These data are especially striking because mutations causing reduced B cell replication and attenuation had minimal effects on the ability of the virus to replicate in macrophages. Thus, norovirus infection of B cells may directly contribute to disease outcome.

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Inactivation of a Foodborne Norovirus Outbreak Strain with Nonthermal Atmospheric Pressure Plasma

Inactivation of a Foodborne Norovirus Outbreak Strain with Nonthermal Atmospheric Pressure Plasma

tively. Our results suggest that NoV can be inactivated by CAPP treatment. The lack of cell culture assays prevents our ability to estimate infectivity. It is possible that some detectable, intact virus particles were rendered noninfectious. We conclude that CAPP treatment of surfaces may be a useful strategy to reduce the risk of NoV transmission in crowded environments. IMPORTANCE Human gastroenteritis is most frequently caused by noroviruses, which are spread person to person and via sur- faces, often in facilities with crowds of people. Disinfection of surfaces that come into contact with infected humans is critical for the prevention of cross-contamination and further transmission of the virus. However, effective disinfection cannot be done easily in mass catering environments or health care facilities. We evaluated the efficacy of cold atmospheric pressure plasma, an innovative airborne disinfection method, on surfaces inoculated with norovirus. We used a clinically relevant strain of norovirus from an outbreak in Germany. Cold plasma was able to inactivate the virus on the tested surfaces, suggesting that this method could be used for continuous disinfection of contaminated surfaces. The use of a clinical strain of norovirus strengthens the reli- ability of our results as it is a strain relevant to outbreaks in humans.

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