1,721,267 research outputs found
Inactivation of Waterborne Viruses by Ozone in Natural Matrices : Proxies for viral inactivation
No full textLE
Data for: Schaub et al., Salt-mediated inactivation of influenza A virus in 1-μl droplets exhibits exponential dependence on NaCl molality
No full text<p><strong>Experimental data</strong></p>
<p>This folder contains the experimental data to the figures shown in the main manuscript and Supporting Information.</p>
<p>Figures 1: inactivation curves for 1- and 2-<span>μ</span>l NaCl droplet experiments at 30% RH + NaCl control (infectivity titer and genomic copy enumeration). "Efflorescence" indicates the time at which efflorescence was first observed.</p>
<p>Figures 1: relative radius of NaCl droplets during evaporation. "Efflorescence" indicates the time at which efflorescence was first observed.</p>
<p>Figures 2: inactivation curves for 1-<span>μ</span>l NaCl, LiCl and NaCl/sucrose droplet experiments at 30 and 65% RH + NaCl and LiCl controls (infectivity titer and genomic copy enumeration). "Efflorescence" indicates the time at which efflorescence was first observed.</p>
<p>Figures 2: relative radius of NaCl and NaCl/sucrose droplets during evaporation. "Efflorescence" indicates the time at which efflorescence was first observed.</p>
<p>Figure 4: virus enumeration (infectivity titer and genomic copies) for virion integrity assay.</p>
<p>Figure S4: inactivation curves for bulk experiments at various NaCl molalities (infectivity titer).</p>
<p>Figures S5: inactivation curves for 1-<span>μ</span>l NaCl droplet experiments at 74% RH (infectivity titer and genomic copy enumeration).</p>
<p>Figure S4 and S7: inactivation curves for bulk experiments at pH 11 (infectivity titer).</p>
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<p><strong>Abbrevations used:</strong></p>
<p>GC = Genomic Copies</p>
<p>LoQ = Limit of Quantification</p>
<p>m = molality (mol/kg H2O)</p>
<p>PFU = Plaque Forming Unit</p>
<p>ul = microliter</p>
Effect of wastewater treatment and environmental exposure on an enterovirus population
No full textThe presence of viruses in recreational water can present a risk for human health and wastewater effluent is a source of virus in the environment. Their persistence in the environment influences their probability to find a new host. Studies have shown that external stressors can select for viruses that are more persistent under these stress conditions. The goal of this PhD was to understand how wastewater treatment and exposure to the environment modifies the community composition of enteroviruses in the water. It assessed specifically the effect of activated sludge and chlorination. The first step was to develop a method to measure the infectious concentration eight of the most abundant enterovirus genotypes in a wastewater sample. Using this method, the changes in population composition when going through activated sludge and chlorination were described. Finally, the diversity in environmental persistence of the enterovirus populations was assessed.
Overall, this thesis contributes to a better understanding of the variability of responses to sewage treatment and environmental exposure that exists among a population of enteroviruses. It highlights particularly persistent genotypes, and shows the importance of considering the diversity that exists among enterovirus genotypes when predicting the effect of an inactivating treatment or environmentally-associated stressor.LC
Toward biocontrol of waterborne pathogens: contributions of protists to virus removal and associated mechanisms
No full textHuman viruses are widespread in the water environment and pose a risk to human health. Wastewater effluents represent the main source of viruses discharge in the environment, leading to contamination of aquatic ecosystems. Viral pathogens can persist on the long- term in these ecosystems and cause human viral infections via water or food. Many studies on inactivation of viruses using UV, heat or chlorine have been conducted. However, the control of viruses by microorganisms, such as bacteria and protists, has only been partially studied. The removal or inactivation of viruses by grazers is a challenging field of study as this natural process might be exploited to engineer water treatment biological solutions. My thesis aims at understanding by which mechanisms, and under which conditions, protists control human viral pathogens, and to design or improve water treatment solutions based on microbial control of viral pathogens by protozoa. The expected outcomes are (i) the determination of the contribution of protists to human viral control in surface water and how this is affected by abiotic and biotic factors, (ii) an investigation of which virus species are affected and why the susceptibility to grazing is different among human viruses, (iii) an understanding of the underlying mechanisms of viral control by protists and (iv) a proposition of design, or improvement, of a water disinfection treatment based on grazing of human viruses by protists. This PhD will provide knowledge on how human viral pathogens are controlled by protists in aquatic ecosystems and how this could be used in man-made water treatment systems.LC
Virus Inactivation during Water Treatment : the Role of Virus Aggregation and the Disinfection Potential of Sunlight
No full textVirus removal and inactivation is still a major challenge for water treatment facilities in both industrialised nations and developing countries. This may seem surprising as chlorine disinfection started to spread broadly over a century ago. However, many viruses are more resistant to disinfection by chlorine and other oxidants than other pathogens. Additionally, some viruses are known to be particularly difficult to disinfect by UV. Finally, viruses are extremely small (18-120 nm diameter), which makes sedimentation impossible and filtration difficult. As no real-time methods exist to enumerate viruses, disinfectant doses are based on lab experiments typically conducted with dispersed viruses. However, viruses in wastewater and natural environments can be present as aggregates. Previous studies have shown that aggregates protect viruses from disinfection, but it remains unclear what renders these aggregates more resistant compared to dispersed viruses. In order to elucidate this observation, aggregates of bacteriophage MS2 of well-defined sizes up to 1 μm diameter were produced by lowering the solution pH, and aggregates were inactivated by peracetic acid (PAA). Aggregates were re-dispersed before enumeration to obtain the residual number of individual infectious viruses. In contrast to enumerating whole aggregates, this approach allowed an assessment of disinfection efficiency which remains applicable even if the aggregates disperse in post-treatment environments. Aggregation reduced the apparent inactivation rate constants 2-6 fold, depending on the aggregate size. The larger the aggregate and the higher the PAA concentration, the more pronounced was the inhibitory effect of aggregation on disinfection. A reaction diffusion model, developed to simulate aggregate disinfection, showed that the inhibitory effect of aggregation arises from consumption of the disinfectant within the aggregate, but that diffusion of the disinfectant into the aggregates is not a rate-limiting factor. Aggregation therefore has a large inhibitory effect if highly reactive disinfectants are used, whereas inactivation by mild disinfectants is less affected. This finding leads to the counterintuitive notion that mild disinfectants, rather than aggressive ones, should be used when virus aggregates are present. During UV disinfection, viruses disinfection curves frequently exhibit a tailing after an initial exponential decay. Aggregation, light shielding, genome recombination or resistant virus sub-populations were proposed as explanations. However, none of these options has conclusively been demonstrated. We investigated how aggregation affects virus inactivation by UV254 in general, and the tailing phenomena in particular. A similar experimental set-up was used as described above with the difference that UV254 disinfection was applied instead of PAA addition. Results showed that initial inactivation kinetics were similar for viruses incorporated in aggregates and dispersed viruses. However, aggregated viruses started to tail more readily than dispersed ones. Neither light shielding, nor the presence of resistant sub-populations could account for the tailing. Instead, tailing was consistent with genome recombination arising as a result of the simultaneous infection of the host by several impaired viruses. We argue that UV254 treatment of aggregates permanently fuses a fraction of viruses, which increased the likelihood of multiple infection of a host cell and ultimately enables the production of infective viruses via recombination. Our results suggest that UV disinfection followed by the addition of a mild disinfectant should yield efficient disinfection for waters containing viral aggregates. Outside Europe and North America wastewater is rarely efficiently treated as treatment costs are often too high and additionally require highly-skilled personnel. To mitigate this issue, waste stabilisation ponds (WPSs) are a viable option because both construction and maintenance are inexpensive and easy to be executed. Pathogen inactivation in these pond systems is mainly attributed to sunlight. Although viruses are among the most resistant pathogens, little is known about sunlight-mediated inactivation mechanisms for these pathogens. Viruses can either be inactivated directly by UV light absorption by the viral genomes, or indirectly via light absorption by sensitizers. The excited sensitizers lead to the formation of reactive species, typically oxidants, which can further react with the viruses and lead to inactivation. Two bacteriophages were chosen as model viruses to investigate these inactivation mechanisms; phiX174, which is resistant to oxidants, and MS2, which is relatively resistant to direct UV inactivation. The efficiency of direct inactivation by solar UVB light was determined, and the rate constants associated with the inactivation by four potentially important reactive species present in sunlit surface waters (singlet oxygen, triplet state organic matter, hydroxyl and carbonate radicals) were quantified. A model was developed that computes the contribution of each of these inactivation mechanisms for ponds with different depths and solution parameters. Direct inactivation was found to be the major inactivation mechanism for phiX174 and also X contributed importantly to inactivation of MS2. Singlet oxygen was the most important reactive species for both virus below 0.5 m. Nevertheless, it did not contribute significantly to the overall inactivation of phiX174. These results suggest that maturation ponds should either be shallow or continuously-mixed to achieve good disinfection results. They furthermore demonstrate that virus inactivation can be reasonably approximated based on easy to determine solution parameters, along with information regarding the sensitivity to viruses toward direct inactivation and few selected reactive species.LE
Inactivation of waterborne viruses by ozone: Kinetics and mechanisms
No full textThe growing world population, in conjunction with climate change, cases the global water de-mand to increase. It is, therefore, crucial to protect existing water resources from chemical pollution and contamination by pathogens. An increasingly popular strategy to meet increased water demand is pota-ble water reuse, which uses wastewater effluent as the water source and treats it to such an extent that it is safe to drink. However, this practise may encompass risks for human health if the treatment train does not ensure a sufficient removal of chemical and microbial contaminants. In the context of both wa-ter and wastewater treatment, ozonation has emerged as an efficient treatment method for the control of pathogens, the abatement of organic micropollutants, and the removal of taste and odor compounds. Despite its popularity, information on the inactivation of waterborne viruses by ozone is scarce.
The aim of this thesis was to investigate the kinetics and mechanisms of inactivation of water-borne viruses by ozone. In a first step, the inactivation kinetics of a suite of human viruses and commonly used surrogates (bacteriophages) were determined in well-controlled buffer systems. To this end, we developed a method to control O3 decay in batch reactors. This allowed us to measure virus inactivation as a function of low ozone exposures. The resulting inactivation rate constant (kO3-virus) differed between the virus species studied, but all kO3-virus fell within a narrow range of 105-106 M-1s-1. These high inactivation rate constant indicate that ozone is efficient to inactivate waterborne virus. Increases in temperature and pH resulted in an increased kO3-virus, though the effect was relatively minor.
To determine if more complex, natural water matrices influence virus inactivation by ozone, we investigated the virucidal efficacy of ozone in two surface waters and a secondary wastewater effluent. While inactivation kinetics as a function of ozone exposure initially corresponded well to those observed in buffer solutions, the inactivation curve tailed off at higher ozone exposures. Furthermore, because it is not possible to measure virus inactivation during water treatment in real-time, we tested different if â easy-to-measureâ proxies can be used to track virus inactivation. We determined that the applied specif-ic ozone dose, the reduction in UV254, or the abatement of carbamazepine all correlated to virus inactiva-tion, though some proxy-inactivation relationships were not universal but depended on the water type. The proxies were validated in a pilot-scale ozonation reactor treating Lake Zurich water, and were found to provide good estimates of virus inactivation.
Finally, an immunostaining assay was developed to observe how ozonation affects crucial steps in the life cycle of echovirus 11, a representative of the Enterovirus genus. Specifically, we investigated if ozone alters the ability of the virus to enter the host cells, and if it prevents the viral genome from replicating. Preliminary results indicate a loss of internalization after ozone treatment as well as genome replication.
In conclusion, this thesis provides new information on the efficacy and mechanisms of ozone as an inacti-vating treatment for waterborne viruses, and it delivers tools to monitor virus inactivation during water and wastewater treatment in real-time.LE
Characterization of bacterial communities in Lake Geneva by comparing genetic and physiological methods
No full textOver the last century, the level of atmospheric CO2 has increased to the highest concentrations on Earth within the past 800'000 years. Current predictions anticipate that the effects of greenhouse gases will lead to a rise in air temperature ranging between 1.4 and 5.8°C. Oceans and freshwater ecosystems absorb large quantities of CO2, but are sensitive to global climate change that directly influences water temperature and pH. Specifically, phytoplankton accounts for approximately 50% of the total photosynthesis on Earth, and contributes to the mobilization of CO2 through sinking or transferring fixed carbon to deeper water layers and sediments. Bacteria are among the most abundant entities in plankton and play a major role on the biological pump for the cycling of carbon and other elements. In order to understand and anticipate the response of aquatic ecosystems to climate change, we need to characterize how planktonic organisms respond and adapt to environmental change. In this project, we will merge microbial ecology and genomics with the ultimate goals of (i) characterizing current ecological niches of the operational taxonomic units highlighted in bacteria populations of Lake Geneva, (ii) identifying candidate adaptive genes responsible for adaptation of freshwater bacterial communities to contrasting freshwater habitats, (iii) projecting current bacteria distributions as a function of the expected change and (iv) identifying possible alterations in ecosystem functioning and services as a function of climate change. By doing this, we expect to contribute expanding our ability to characterize ecological niches using genetic data and sensitizing society about the importance of protecting freshwater ecosystems.SIE-SLE
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