Influenza A virus (subtype H3N2) causes seasonal human influenza and is included as a component of influenza vaccines. The majority of vaccine viruses are isolated and propagated in eggs, which commonly results in amino acid substitutions in the haemagglutinin (HA) glycoprotein. These substitutions can affect virus receptor-binding and alter virus antigenicity, thereby, obfuscating the choice of egg-propagated viruses for development into candidate vaccine viruses. To evaluate the effects of egg-adaptive substitutions seen in H3N2 vaccine viruses on sialic acid receptor-binding, we carried out quantitative measurement of virus receptor-binding using surface biolayer interferometry with haemagglutination inhibition (HI) assays to correlate changes in receptor avidity with antigenic properties. Included in these studies was a panel of H3N2 viruses generated by reverse genetics containing substitutions seen in recent egg-propagated vaccine viruses and corresponding cell culture-propagated wild-type viruses. These assays provide a quantitative approach to investigating the importance of individual amino acid substitutions in influenza receptor-binding. Results show that viruses with egg-adaptive HA substitutions R156Q, S219Y, and I226N, have increased binding avidity to α2,3-linked receptor-analogues and decreased binding avidity to α2,6-linked receptor-analogues. No measurable binding was detected for the viruses with amino acid substitution combination 156Q+219Y and receptor-binding increased in viruses where egg-adaptation mutations were introduced into cell culture-propagated virus. Substitutions at positions 156 and 190 appeared to be primarily responsible for low reactivity in HI assays with post-infection ferret antisera raised against 2012–2013 season H3N2 viruses. Egg-adaptive substitutions at position 186 caused substantial differences in binding avidity with an insignificant effect on antigenicity.

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Influenza virus infection is a significant cause of morbidity and mortality worldwide. The surface antigens of influenza virus change over time blunting both naturally acquired and vaccine induced adaptive immune protection. Viral antigenic drift is a major contributing factor to both the spread and disease burden of influenza. The aim of this study was to develop better infection models using clinically relevant, influenza strains to test vaccine induced protection. CB6F1 mice were infected with a range of influenza viruses and disease, inflammation, cell influx, and viral load were characterized after infection. Infection with circulating H1N1 and representative influenza B viruses induced a dose-dependent disease response; however, a recent seasonal H3N2 virus did not cause any disease in mice, even at high titers. Viral infection led to recoverable virus, detectable both by plaque assay and RNA quantification after infection, and increased upper airway inflammation on day 7 after infection comprised largely of CD8 T cells. Having established seasonal infection models, mice were immunized with seasonal inactivated vaccine and responses were compared to matched and mismatched challenge strains. While the H1N1 subtype strain recommended for vaccine use has remained constant in the seven seasons between 2010 and 2016, the circulating strain of H1N1 influenza (2009 pandemic subtype) has drifted both genetically and antigenically since 2009. To investigate the effect of this observed drift on vaccine induced protection, mice were immunized with antigens from A/California/7/2009 (H1N1) and challenged with H1N1 subtype viruses recovered from 2009, 2010, or 2015. Vaccination with A/California/7/2009 antigens protected against infection with either the 2009 or 2010 strains, but was less effective against the 2015 strain. This observed reduction in protection suggests that mouse models of influenza virus vaccination and infection can be used as an additional tool to predict vaccine efficacy against drift strains.

Discovering catalysts that can decompose N2O at low temperatures represents a major challenge in modern catalysis. The effect of preparative route on N2O-decomposition activity has been examined for a PrBaCoO3 perovskite catalyst. Initially, a citric acid preparation was utilised where the A site ratio was altered in order to increase phase purity. Comparable compositions were then prepared by an oxalic acid precipitation method and by a supercritical anti-solvent technique to produce perovskites with a higher surface area (> 30 m 2 g -1 ). By altering the A site ratio it was possible to reduce the temperature required to produce a pure phase perovskite whilst maintaining a higher-surface area.The use of the different preparation methods resulted in perovskites with varying properties, as determined by N2 adsorption, XPS, O2-TPD and H2-TPR. This work confirms the importance of lattice oxygen species that have high oxygen mobility for enhanced decomposition of N2O, as oxygen recombination is considered the rate-limiting step. Here, the formation of molecular oxygen is limited by surface adsorbed O species being within a distance at which oxygen recombination is possible. The most active PrBaCo-based catalyst did not have the highest percentage of lattice oxygen as shown by XPS, however, the catalytic activity could be correlated to the mobile oxygen species and high surface area. The PrBaCo-based catalyst prepared by supercritical anti-solvent converted 50 % of the N2O present in the feed (T50) at 410 °C, which represents a significant improvement over reported catalytic performance measured under similar conditions.

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Humans are the sole reservoir for mumps virus (MuV), the causative agent of mumps. No animal model currently exists; therefore, in vivo knowledge of the virus is limited. Ferrets were assessed for their susceptibility to MuV based on their success as a model for influenza. We infected ferrets with clinical or attenuated vaccine MuVs by the nasal route and demonstrated evidence of immunogenicity in these animals with generation of a serum antibody response specific to MuV infection and cytokine production consistent with infection. However, no live virus or viral RNA was detected in nasal washes, oral swabs, urine, faeces or tissue homogenates, and no animals exhibited clinical signs. We suggest results to be obtained from ferrets are limited in fundamental in vivo MuV research and that they may not be a suitable animal model for this virus.

The presence of microplastics in environmental compartments is generally recognized as a (potential) health risk. Many papers have been published on the abundance of microplastics at various locations around the globe, but only limited knowledge is available on possible mitigation routes. One of the mitigation routes is based on the choice of plastic materials used for products that may unintentionally end up in the environment. As a first approach, this paper presents a method to calculate the tendency of polymers to form microplastics, based on their mechanical and physical properties. A MicroPlastic Index (MPI) that correlates the microplastic formation to polymer properties is defined for both impact and wear of polymers via a theoretical particle size and the energy required to form these particles. A first comparison between calculated and experimental particle size is included. The MPI for impact and wear follow the same trend. Finally, these MPIs are correlated to the respective abundance of the microplastics in the environment, corrected for global production of the corresponding polymers: the higher the MPI, the more microplastics are found in the environment. Thus, the MPI can be used as a basis for choice or redesign of polymers to reduce microplastic formation.

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