Virus

Summary

A virus is a submicroscopic infectious agent that replicates only inside the living cells of an organism. Viruses infect all life forms, from animals and plants to microorganisms, including bacteria and archaea. Since Dmitri Ivanovsky's 1892 article describing a non-bacterial pathogen infecting tobacco plants and the discovery of the tobacco mosaic virus by Martinus Beijerinck in 1898, more than 11,000 of the millions of virus species have been described in detail. Viruses are found in almost every ecosystem on Earth and are the most numerous type of biological entity. The study of viruses is known as virology, a subspeciality of microbiology. When infected, a host cell is often forced to rapidly produce thousands of copies of the original virus. When not inside an infected cell or in the process of infecting a cell, viruses exist in the form of independent viral particles, or virions, consisting of (i) the genetic material, i.e., long m

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Surface modification of PES virus filtration membrane

Claire Roulin

Virus filtration by size exclusion is a robust means of eliminating viruses in blood or pharma products. Porous polymer membranes with a narrow size distribution are used to allow passage of the protein product but retain viruses. The chosen polymer must resist process-induced physical and chemical wear and is therefore generally inert and hydrophobic material. When filtrating potentially heterogeneous products such as IgG from pooled blood samples, protein adsorption on the polymer surface causes high fouling. This eventually blocks the filter and reduces total filtration volume. A solution to this adsorption problem is to graft a hydrophilic gel-like polymer layer on the membrane inner surface to reduce protein adsorption. The surface properties are thus changed while retaining the stability of the bulk polymer. The grafting was initiated with an electron beam, which creates free radicals by unspecific scission of the polymer backbone through electron irradiation. Two acrylate monomers were used for polymerization, a monofunctional monomer and a bifunctional one, used as a crosslinker to form the gel structure. Two different grafting method were tested. The first grafting method is simultaneous grafting, where the membrane is impregnated with the monomer solution then irradiated. Initiation and polymerization thus occur almost simultaneously. The grafted membrane properties were assessed using flow measurements, protein adsorption tests, FTIR absorbance measurements, virus retention tests and filter integrity tests. Comparing the various grafting approaches, it can be seen that simultaneous grafting lowers considerably protein adsorption, to the price of a highly reduced buffer flow. These filters therefore run slowly but can process more volume before fouling. The sequential grafting method using peroxides as initiators did not show significant filtration improvements compared to the reference membrane when the solution with monomer and crosslinker was used. However, when only monofunctional monomer was used for peroxidation grafting, the protein filtration capacity was increased with limited buffer flow loss. Generally, the sequential method is interesting for graft polymerization of porous membranes because it allows higher degree of grafting and the versatile grafting parameters involved give many development options depending on the application

2010

The aim of this study was to determine the difference in disinfection between aggregated and dispersed virus. Bacteriophage MS2 was chosen as a surrogate for enteric virus. The first part of this project consisted of characterizing the aggregation of MS2 and the second part examined differences in the disinfection of aggregated and dispersed virus solutions. It was shown that MS2 only aggregated at a pH below its isoelectric point when the solution ionic strength was below 50 mM. At neutral pH, high ionic strength and CaCl2 did not cause aggregation. High ionic strength showed inhibition of aggregation at low pH. Aggregation was also influenced by the choice of buffer. The effect of the solution chemistry on the extent of aggregation at pH 3 was the following: acetic acid (20 mM)>sodium chloride (20 mM)> phosphate buffer (5 mM PO42-, 10 mM NaCl). Disinfection of the virus was thus tested at a pH above and under the isoelectric point at low ionic strength (phosphate buffer and 20 mM NaCl) in order to have dispersed and aggregated MS2 virus, respectively. Ultraviolet light (UV) and peracetic acid (PAA) were the chosen disinfection techniques as they are generally regarded as pH independent. UV showed greater disinfection capacity for the aggregated system than for the mono- dispersed system. Both disinfection curves showed first order kinetics. This observed difference in disinfection rates may not be due to the aggregation state of the virus but to other mechanisms, including the effect of pH on direct and indirect oxidation (by ROS) of amino acids in the virus capsid proteins. This is supported by the fact that UV can penetrate within the virus unlike a chemical disinfectant which must be in physical contact with a virus component for a reaction to take place. In order to test the effect of direct contact by chemical disinfectants, an aggregated and a dispersed solution were spiked with PAA. A difference in the behavior of the disinfection curves in phosphate buffer was observed after an inactivation of 6 logs. The disinfection rate of the aggregated system slowed down (tailing) after some initial amount of disinfection, while the dispersed system was completely disinfected with one disinfection rate. This implies a solution with some large aggregates and many single viruses in the solution. In 20 mM NaCl the disinfection rate of the aggregated virus was much slower than for the dispersed system (kaggregated= 0.0224; kdispersed= 0.0747). Both inactivation curves showed first order kinetics. By applying Grant’s model (1995) an aggregation factor was calculated (b= 1.413). This indicates a very aggregated state with large aggregates.

2009

Susceptibility of Enterovirus B strains to disinfectants and heat

Simon Meister

The susceptibility of waterborne viruses to different inactivating treatments is acknowledged to vary between viruses and even between closely related strains, yet the extent of this variation, or the underlying mechanisms, are not known. Here, different enteroviruses (six strains of coxsackievirus B5 (CVB5), two strains of coxsackievirus B4 (CVB4) and one strain of coxackievirus B1 (CVB1)) were isolated from wastewater. The different viruses were then exposed to disinfectants used in water and wastewater treatment (UV254, free chlorine (FC), chlorine dioxide (ClO2)) and to stressors encountered in the environment (sunlight, temperature). Inactivation kinetics of the environmental isolates were compared with those of laboratory enterovirus strains (CVB5 Faulkner and echovirus 11 Gregory) and MS2 bacteriophage. FC exhibited the greatest variability in inactivation kinetics between different strains, whereas inactivation by UV254 differed only subtly. The variability in inactivation kinetics was greater between serotypes than it was among the seven strains of the CVB5 serotype. MS2 was a conservative surrogate of enterovirus inactivation by UV254, sunlight or heat, but frequently underestimated the disinfection requirements for FC and ClO2. To assess the mechanisms underlying the differing susceptibilities of these viruses to inactivation, we focused on thermal inactivation. Specifically, we extensively analyzed the inactivation of these viruses at 30 and 55°C, and under different conditions of pH and NaCl concentrations. At 30°C, inactivation at neutral pH was slow, but both acidic and alkaline pH enhanced inactivation, and the addition of 1 M NaCl exerted a synergistic inactivating effect. These findings are consistent with RNA cleavage being the main mechanism of inactivation, and genome degradation was experimentally confirmed. At 55°C, salt had a protective effect on all viruses. This was rationalized by calculations of the different protein interaction forces, which demonstrated that increasing concentrations of salt resulted in increasing attractive forces at the capsid pentamer interfaces. At this temperature, major differences in thermoresistance between the viruses were observed, with CVB4 and E11 displaying the lowest thermoresistance, and the CVB5 laboratory strain being less thermoresistant than the CVB5 isolates. These differences could not be explained by a shift in capsid pentamer interaction forces, but likely resulted from mutations located in VP1 pocket region. The importance of the VP1 pocket region was further confirmed by adapting CVB5 to two different temperatures (50 and 55 °C). The thermo-adapted strains exhibited a competitive fitness trade-off compared to control strains, but were significantly more resistant to thermal inactivation. This resistance coincided with the appearance of one or several of four mutations in the VP1 region of the structural proteins. These mutations did not affect the interaction forces at the pentamer interface. Instead, they were located in the VP1 pocket region, confirming the importance of this region in the acquisition of thermotolerance. Overall, these data indicate that the thermostability of a virus can be enhanced by external (matrix) factors, in particular salinity, or by intrinsic (structural) modifications in the VP1 pocket region.

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