Hepatitis C virus infects and perturbs liver stem cells

Hepatitis C virus (HCV) is the leading cause of death from liver disease. How HCV infection causes lasting liver damage and increases cancer risk remains unclear. Here, we identify bipotent liver stem cells as novel targets for HCV infection, and their erroneous differentiation as the potential cause of impaired liver regeneration and cancer development. We show 3D organoids generated from liver stem cells from actively HCV-infected individuals carry replicating virus and maintain low-grade infection over months. Organoids can be infected with a primary HCV isolate. Virus-inclusive single-cell RNA sequencing uncovered transcriptional reprogramming in HCV+ cells supporting hepatocytic differentiation, cancer stem cell development, and viral replication while stem cell proliferation and interferon signaling are disrupted. Our data add a new pathogenesis mechanism—infection of liver stem cells—to the biology of HCV infection that may explain progressive liver damage and enhanced cancer risk through an altered stem cell state

Notes for genera: basal clades of Fungi (including Aphelidiomycota, Basidiobolomycota, Blastocladiomycota, Calcarisporiellomycota, Caulochytriomycota, Chytridiomycota, Entomophthoromycota, Glomeromycota, Kickxellomycota, Monoblepharomycota, Mortierellomycota, Mucoromycota, Neocallimastigomycota, Olpidiomycota, Rozellomycota and Zoopagomycota)

Compared to the higher fungi (Dikarya), taxonomic and evolutionary studies on the basal clades of fungi are fewer in number. Thus, the generic boundaries and higher ranks in the basal clades of fungi are poorly known. Recent DNA based taxonomic studies have provided reliable and accurate information. It is therefore necessary to compile all available information since basal clades genera lack updated checklists or outlines. Recently, Tedersoo et al. (MycoKeys 13:1--20, 2016) accepted Aphelidiomycota and Rozellomycota in Fungal clade. Thus, we regard both these phyla as members in Kingdom Fungi. We accept 16 phyla in basal clades viz. Aphelidiomycota, Basidiobolomycota, Blastocladiomycota, Calcarisporiellomycota, Caulochytriomycota, Chytridiomycota, Entomophthoromycota, Glomeromycota, Kickxellomycota, Monoblepharomycota, Mortierellomycota, Mucoromycota, Neocallimastigomycota, Olpidiomycota, Rozellomycota and Zoopagomycota. Thus, 611 genera in 153 families, 43 orders and 18 classes are provided with details of classification, synonyms, life modes, distribution, recent literature and genomic data. Moreover, Catenariaceae Couch is proposed to be conserved, Cladochytriales Mozl.-Standr. is emended and the family Nephridiophagaceae is introduced

Performance of distinct microbial based solutions in a Campylobacter infection challenge model in poultry

Abstract Background Antibiotic growth promoters (AGPs) are commonly used within poultry production to improve feed conversion, bird growth, and reduce morbidity and mortality from clinical and subclinical diseases. Due to the association between AGP usage and rising antimicrobial resistance, the industry has explored new strategies including the use of probiotics and other microbial-based interventions to promote the development of a healthy microbiome in birds and mitigate against infections associated with food safety and food security. While previous studies have largely focused on the ability of probiotics to protect against Clostridium perfringens and Salmonella enterica, much less is known concerning their impact on Campylobacter jejuni, a near commensal of the chicken gut microbiome that nevertheless is a major cause of food poisoning in humans. Results Here we compare the efficacy of four microbial interventions (two single strain probiotics, the bacterium—Pediococcus acidilactici, and the yeast—Saccharomyces cerevisiae boulardii; and two complex, competitive exclusion, consortia—Aviguard and CEL) to bacitracin, a commonly used AGP, to modulate chicken gut microbiota and subsequently impact C. jejuni infection in poultry. Cecal samples were harvested at 30- and 39-days post hatch to assess Campylobacter burden and examine their impact on the gut microbiota. While the different treatments did not significantly decrease C. jejuni burden relative to the untreated controls, both complex consortia resulted in significant decreases relative to treatment with bacitracin. Analysis of 16S rDNA profiles revealed a distinct microbial signature associated with each microbial intervention. For example, treatment with Aviguard and CEL increased the relative abundance of Bacteroidaceae and Rikenellaceae respectively. Furthermore, Aviguard promoted a less complex microbial community compared to other treatments. Conclusions Depending upon the individual needs of the producer, our results illustrate the potential of each microbial interventions to serve flock-specific requirements