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Hepatitis E Virus
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Kavita Lole, Prudhvi Lal Bhukya, Bangari Haldipur
Stability of HEV in different environmental conditions and in food items is not known. Enteric viruses are known to persist for a longer period in water and food and remain infectious for a prolonged period. Virus stability is affected by various environmental conditions and factors such as temperature, moisture, and pH. Detection of enteric viruses in food is difficult due to low levels of virus and complexity of food matrices. The presence of inhibitors in the samples can also mask the detection. Studies on HEV survival are limited since there is no robust cell culture or small animal model for evaluating viral viability. Being an enteric virus, it has the ability to withstand acidic conditions in the stomach. It is proposed that as HEV capsid protein undergoes conformational changes when subjected to low pH, it may provide more stability to the virus allowing it to retain its infectivity.213 There are some studies documenting the stability of the virus in different cooking conditions. Emerson et al.36 monitored infectivity of three strains of HEV (two HEV-1 and one HEV-2 strains) by incubating virus suspensions at 45°C–70°C for 1 hour and checked infectivity in HepG2/C3A (human hepatoma) cells. It was noted that treatment at 56°C for 15 minutes was effective in inactivation of 95% of virus, while 60 minute treatment could kill 99% infectious virus. There was 100% inactivation of the virus when samples were kept for 1 hour at 66°C and at 70°C for 1 hour. Authors also noted that HEV can remain stable in frozen conditions for several years. Tanaka et al. used composite infectivity in cell culture and PCR assay (ICC-PCR) for viability testing.193 It involved infection of cultured PLC/PRF/5 cells with the virus followed by quantitative PCR. These experiments showed that treatment at 70°C for 10 minutes can completely inactivate the virus. Yunoki et al.214 showed that treatment of HEV-3 and HEV-4 in 1X phosphate-buffered saline at 60°C for 30 minutes was effective in eliminating 2.4–3.7 log virus, while virus suspended in a 25% human serum albumin solution showed only 1.0 and 2.2 log reductions after treatment for 5 hours at 60°C. These results indicated that virus is heat resistant when suspended in enriched medium.
Human Gut Microbiota–Transplanted Gn Pig Models for HRV Infection
Published in Lijuan Yuan, Vaccine Efficacy Evaluation, 2022
The mean relative abundance of phyla between UHGM pig LIC samples and the infant stool sample (PM25) was similar, which was as expected. However, HHGM pig samples differed from their infant donor (SV14). Community structure may have been different between the human donor and pigs because of the influence of different environments, differences in diet, lack of natural microbial succession in the pigs, or differences in host genetics (Schmidt et al., 2011). The phylum- and genus-level differences between HHGM and UHGM pigs at both time points warrant further study to assess the influences of these OTUs on the host immune response. In HHGM pigs, after VirHRV challenge, there was a decrease in the relative abundance of Firmicutes, similar to previous observations (Zhang et al., 2014). Although we did not sample pigs without AttHRV vaccination, human studies have shown that rotavirus vaccination does not have any major effects on the gut microbiota of children (Ang et al., 2014; Garcia-Lopez et al., 2012). Similar to a human study, HHGM pigs had an increased mean relative abundance of Bacteroides after rotavirus infection (Zhang et al., 2009). Bacteroides and Lactobacillus species have been shown to modify cell-surface glycans in human intestinal cultured cells, effectively blocking rotavirus infection (Varyukhina et al., 2012). This may partially explain why HHGM pigs had decreased viral shedding when compared to UHGM pigs. In agreement with a previous study, we also observed a decrease in levels of Streptococcus in HHGM pigs after the rotavirus challenge (Zhang et al., 2014). There is limited data on mechanisms by which microbiota directly influences enteric virus infectivity. Microbiota may modify the cell surface or bind to pathogens. In vitro experiments have demonstrated soluble factors from Bacteroides thetaiotaomicron and Lactobacillus casei can increase cell-surface galactose and block rotavirus infection (Varyukhina et al., 2012). Poliovirus binds bacterial surface polysaccharides, which enhances virion stability and cell attachment, and may enhance transmission (Robinson et al., 2014). Gnotobiotic pigs colonized with E. coli Nissle 1917 (EcN) had lower viral shedding titers, which the authors speculated was because EcN bound to HRV particles (Kandasamy et al., 2016).
Introduction to water-related hazards *
Published in Jamie Bartram, Rachel Baum, Peter A. Coclanis, David M. Gute, David Kay, Stéphanie McFadyen, Katherine Pond, William Robertson, Michael J. Rouse, Routledge Handbook of Water and Health, 2015
Stéphanie McFadyen, William Robertson
It is important here to make the distinction between hazard and risk. As noted above, hazard refers to potential sources of adverse health effects or harm. Risk, on the other hand, is the likelihood or probability that a person may suffer adverse health effects or be harmed if exposed to a hazard. As a simple example, consider lightning strikes: lightning is a massive electrostatic discharge and is clearly a deadly hazard, yet the chances of a person being killed by lightning depend on the amount of time spent outdoors and the presence of lightning-proof buildings. In a developed country such as Canada for example, the risk is generally less than one in a million but it can be higher in developing countries (Mills et al., 2008). In a drinking water context, the path from hazard to risk can be direct in a low-resource setting where there is little to no treatment or management of a water source, or it can involve many steps to understand the impacts of risk mitigation measures. Consider an enteric virus such as norovirus, known to be a hazard in drinking water. Noroviruses cause acute gastrointestinal upset (nausea, vomiting, diarrhea) and their routes of transmission include person-to-person contact as well as contaminated water amongst others. To quantify the water-related risk from norovirus, information on concentrations in source water, the impact of water treatment barriers and a pathogen specific dose–response model is applied in a process known as microbiological risk assessment (WHO, 2011; Health Canada, 2011). More detail on this approach can be found in Chapter 56. While working to quantify the water-related risk from norovirus, it must be clearly understood that interventions to control water-borne exposures to this virus may not affect the overall burden of disease if other significant exposures routes such as food or person-to-person transmission are not controlled. In the case of pathogenic microorganisms the immune status of the exposed population or individual determines their vulnerability to infection and illness. Some recognized groups in this category include children, pregnant women, the elderly and persons with compromised or suppressed immune systems. In the case of chemicals, exposure during susceptible times of development (e.g. the developing foetus or in young and children) may result in long-lasting harm. In all cases, the most significant effects are felt when the hazard, a vulnerable population or individual and environmental considerations overlap (Figure 2.1); not surprisingly, this will also be the zone where risk is at its highest. Exposures and ensuing risks are addressed in other parts of the handbook.
Validation studies for germ-free Smad3-/- mice as a bio-assay to test the causative role of fecal microbiomes in IBD
Published in Gut Microbes, 2020
Jisun Paik, Stacey Meeker, Charlie C. Hsu, Audrey Seamons, Olesya Pershutkina, Jessica M. Snyder, Thea Brabb, Lillian Maggio-Price
In future studies, we want to identify causative microbiomes responsible for IBD and CAC. Because Smad3-/- mice develop severe inflammation in cecum and colon upon colonization with microbiota associated with H. bilis-induced IBD, requiring euthanasia, long-term studies needed for understanding the role of the microbiome in CAC development are not possible using fecal transfer of mouse IBD microbiomes in these mice. Previous studies have reported that an enteric virus, murine norovirus, can replace some of the functions of commensal bacteria in proper immune cell development in the intestines of GF mice.30 Interestingly, mono-colonization with H. bilis, a commensal bacterium in immune-competent mice, prior to fecal transfer from mice with IBD significantly reduced inflammation in both cecum and colon compared to mice that were not mono-colonized prior to fecal transfer in both Smad3+/- and Smad3-/- recipients. Currently, we do not know whether other commensal bacteria can elicit the same suppressive effects on gut inflammation induced by microbiome-transfer into GF mice. Recent studies suggest that another Helicobacter species, Helicobacter hepaticus can induce regulatory T cells in wild type mice in a c-MAF-dependent manner while it induces expansion of Th17 cells in Il10-/- mice,31 suggesting that interactions between microbiota and a host genetic susceptibility promote gut inflammation. Further studies will be needed to determine whether H. bilis mono-colonization alters cancer development at later time points and whether H. bilis mono-colonization suppresses inflammation by changing H. bilis-specific immune responses or if immune responses are generally more attenuated due to previous exposure to this commensal bacterium.
Outcomes and implications of diarrhea in patients with SARS-CoV-2 infection
Published in Scandinavian Journal of Gastroenterology, 2020
Haitao Shang, Tao Bai, Yuhua Chen, Chao Huang, Shengyan Zhang, Pengcheng Yang, Lei Zhang, Xiaohua Hou
A total of 36 diarrhea patients carried out the 2019-nCoV nucleic acid test during diarrhea. Diarrhea occurred earlier with possible longer duration in patients with positive fecal coronavirus than the negative ones. Also, diarrhea patients with positive fecal coronavirus showed longer disease course and hospital stay relative to diarrhea patients with negative fecal coronavirus (Table 3). It indicated a close link between enteric virus carrying and longer course of illness in COVID-19 patients with diarrhea.