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Kohn, T.

Publications and source records attributed to Kohn, T..

20 records · Page 2Linked to original sources

Observed Kinetics of Enterovirus Inactivation by Free Chlorine Is Host Cell-Dependent

The virucidal efficacy of disinfectants is typically assessed by infectivity assay utilizing a single type of host cell. Enteroviruses infect multiple host cells via different entry routes, and each entry route may be impaired to a varying extent by a given disinfectant. Yet, it is not known how the choice of host cells for titration affects the observed inactivation kinetics. Here, we evaluated the inactivation kinetics of echovirus 11 (E11) by free chlorine, ultraviolet (UV) irradiation, and heat, using three different host cells (BGMK, RD, and A549). E11 inactivation by free chlorine occurred at a two-fold greater rate when enumerated on BGMK cells compared to RD and A549 cells. Conversely, a comparable inactivation rate was observed for UV and heat independent of the host cell used. Host cell-dependent inactivation kinetics by free chlorine were also observed for echovirus 7, 9 and 13, and coxsackievirus A9, confirming that this phenomenon is not serotype-specific. Inactivation of E11 was partly caused by a loss in host cell attachment, which was most pronounced for BGMK cells, and which may be promoted by a lack of CD55 attachment receptors on this cell type. Additionally, BGMK cells lack a key subunit of the uncoating receptor, {beta}2M, which may further contribute to the differential inactivation kinetic for this cell type. Consequently, inactivation kinetics of enteroviruses should be assessed using host cells with different receptor profiles. This will yield a more complete understanding of the inactivating power of disinfectants targeting the viral attachment and/or uncoating. Graphic for Table of Contents (TOC) O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=107 SRC="FIGDIR/small/509468v1_ufig1.gif" ALT="Figure 1"> View larger version (21K): org.highwire.dtl.DTLVardef@148461eorg.highwire.dtl.DTLVardef@1f3667corg.highwire.dtl.DTLVardef@cd75a3org.highwire.dtl.DTLVardef@e65616_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

The novel shapeshifting bacterial phylum Saltatorellota

Our current understanding of a free-living bacterium - capable of withstanding a variety of environmental stresses-is represented by the image of a peptidoglycan-armored rigid casket. The making and breaking of peptidoglycan greatly determines cell shape. The cytoplasmic membrane follows this shape, pressed towards the cell wall by turgor pressure. Consequently, bacteria are morphologically static organisms, in contrast to eukaryotic cells that can facilitate shape changes. Here we report the discovery of the novel bacterial phylum Saltatorellota, that challenges this concept of a bacterial cell. Members of this phylum can change their shape, are capable of amoeba-like locomotion and trunk-formation through the creation of extensive pseudopodia-like structures. Two independent Saltatorellota cells can fuse, and they employ various forms of cell division from budding to canonical binary fission. Despite their polymorphisms, members of the Saltatorellota do possess a peptidoglycan cell wall. Their genomes encode flagella and type IV pili as well as a bacterial actin homolog, the saltatorellin. This protein is most similar to MamK, a dynamic filament-forming protein, that aligns and segregates magnetosome organelles via treadmilling. We found saltatorellin to form filaments in both, E. coli and Magnetospirillum gryphiswaldense, leading to the hypothesis that shapeshifting and pseudopodia formation might be driven by treadmilling of saltatorellin.

microbiology↗