Biobehavioral Aspects of the COVID-19 Pandemic: A Review.

Objective: This review highlights the scope and significance of the coronavirus disease 2019 (COVID-19) pandemic with a focus on biobehavioral aspects and critical avenues for research.

Methods: A narrative review of the published research literature was undertaken, highlighting major empirical findings emerging during the first and second waves of the COVID-19 pandemic.

Results: Interactions among biological, behavioral, and societal processes were prominent across all regions of the globe during the first year of the COVID-19 emergency.

Microbiology for the masses: teaching concepts and skills for a general audience.

Microbes are extraordinarily talented and diverse: they can perform a multitude of tasks and live in a variety of situations. The impact of diverse microbes upon society and the environment can be used to teach students critical skills for a variety of careers.

Enterohemorrhagic Escherichia coli O157:H7 gene expression profiling in response to growth in the presence of host epithelia.

Background: The pathogenesis of enterohemorrhagic Escherichia coli (EHEC) O157:H7 infection is attributed to virulence factors encoded on multiple pathogenicity islands. Previous studies have shown that EHEC O157:H7 modulates host cell signal transduction cascades, independent of toxins and rearrangement of the cytoskeleton. However, the virulence factors and mechanisms responsible for EHEC-mediated subversion of signal transduction remain to be determined.

Probiotics prevent enterohaemorrhagic Escherichia coli O157:H7-mediated inhibition of interferon-gamma-induced tyrosine phosphorylation of STAT-1.

Enterohaemorrhagic Escherichia coli (EHEC) O157:H7 inhibits interferon (IFN)-gamma-stimulated tyrosine phosphorylation of signal transducer and activator of transcription (STAT)-1 in epithelial cells. We determined the effects of probiotics on EHEC-mediated disruption of IFN-gamma-stimulated STAT-1 activation in epithelial cell lines. Confluent Intestine 407, HEp-2 and Caco-2 epithelial cells were pre-treated (3 h) with either probiotics or surface-layer proteins derived from Lactobacillus helveticus R0052 prior to infection with EHEC O157:H7 strain CL56 (m.

Escherichia albertii and Hafnia alvei are candidate enteric pathogens with divergent effects on intercellular tight junctions.

Attaching-effacing lesion-inducing Escherichia albertii and the related, but non-attaching-effacing organism, Hafnia alvei, are both implicated as enteric pathogens in humans. However, effects of these bacteria on epithelial cells are not well-characterized. Related enteropathogens, including enterohemorrhagic Escherichia coli O157:H7, decrease epithelial barrier function by disrupting intercellular tight junctions in polarized epithelia.

Multiple seropathotypes of verotoxin-producing Escherichia coli (VTEC) disrupt interferon-gamma-induced tyrosine phosphorylation of signal transducer and activator of transcription (Stat)-1.

Verotoxin-producing Escherichia coli (VTEC) O157:H7 inhibits interferon-gamma-stimulated tyrosine phosphorylation of signal transducer and activator of transcription (Stat)-1 in epithelial cells, independent of Verotoxins and the locus of enterocyte effacement pathogenicity island. Although E. coli O157:H7 is the major cause of disease in humans, non-O157:H7 VTEC also cause human disease.

Conditioned medium from enterohemorrhagic Escherichia coli-infected T84 cells inhibits signal transducer and activator of transcription 1 activation by gamma interferon.

Gamma interferon (IFN-gamma) is a cytokine important to host defense which can signal through signal transducer and activator of transcription 1 (Stat1). Enterohemorrhagic Escherichia coli (EHEC) modulates host cell signal transduction to establish infection, and EHEC serotypes O113:H21 and O157:H7 both inhibit IFN-gamma-induced Stat1 tyrosine phosphorylation in vitro. The aim of this study was to delineate both bacterial and host cell factors involved in the inhibition of Stat1 tyrosine phosphorylation.