In cells infected with mesogenic or lentogenic strain of Newcastle disease virus the level of neuraminidase and hemagglutinin activities sharply decreased after the addition of cycloheximide. With two velogenic strains such decreases did not occur. The infected cells were labelled with 14C-amino acids (leucine or valine) and further incubated with an excess of unlabelled precursor. Polyacrylamide gel analysis revealed a decrease of the peak correspondig to the "large" glycoprotein after the chase in cells infected with meso- or lentogenic strain (Beaudette, B1). In the cells infected with velogenic strains (Italia, Herts) no such decrease was observed. The degradation of the "large" glycoprotein as the cause of the decrease of hemagglutinin and neuraminidase activities in cycloheximide-treated cells and its possible relation to virulence is discussed.
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Bull Math Biol
January 2025
Department of Mathematics, University of Manitoba, 340 UMSU University Centre, Winnipeg, MB, R3T 2N2, Canada.
The immune checkpoint inhibitor, anti-programmed death protein-1 (anti-PD-1), enhances adaptive immunity to kill tumor cells, and the oncolytic virus (OV) triggers innate immunity to clear the infected tumor cells. We create a mathematical model to investigate how the interaction between adaptive and innate immunities under OV and anti-PD-1 affects tumor reduction. For different immunity strength, we create the corresponding virtual baseline patients and cohort patients to decipher the major factors determining the treatment outcome.
View Article and Find Full Text PDFArch Microbiol
January 2025
Department of Microbiology, Faculty of Biotechnology and Biomolecular Sciences, Universiti Putra Malaysia, Serdang, Selangor, 43400, Malaysia.
Bacteriophages produce endolysins at the end of the lytic cycle, which are crucial for lysing the host cells and releasing virion progeny. This lytic feature allows endolysins to act as effective antimicrobial alternatives when applied exogenously. Staphylococcal endolysins typically possess a modular structure with one or two enzymatically active N-terminal domains (EADs) and a C-terminal cell wall binding domain (CBD).
View Article and Find Full Text PDFHepatol Commun
February 2025
University Grenoble Alpes, Inserm U 1209, CNRS UMR 5309, Institute for Advanced Biosciences, Grenoble, France.
Background: Hepatitis B is a liver infection caused by HBV. Infected individuals who fail to control the viral infection develop chronic hepatitis B and are at risk of developing life-threatening liver diseases, such as cirrhosis or liver cancer. Dendritic cells (DCs) play important roles in the immune response against HBV but are functionally impaired in patients with chronic hepatitis B.
View Article and Find Full Text PDFMol Biol Cell
January 2025
Institute for Biochemistry & Research Center for Emerging Infections and Zoonoses (RIZ), University of Veterinary Medicine Hannover, Hannover, Germany.
Tetraspanins (Tspans) are transmembrane proteins that coordinate life cycle steps of viruses from distinct families. Here, we identify the human Tspan10 and Tspan15, both members of the TspanC8 subfamily, as replication factors for alphavirus Venezuelan equine encephalitis virus (VEEV) in astrocytoma cells. Pharmacological inhibition and siRNA-mediated silencing of TspanC8 interactor a disintegrin and metalloproteinase 10 (ADAM10) reduced VEEV infection.
View Article and Find Full Text PDFInfect Immun
January 2025
Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, USA.
Streptococcal pyogenic exotoxins (Spe proteins) secreted by (group A , GAS) are responsible for scarlet fever and streptococcal toxic shock syndrome. Most Spes are superantigens that cause excessive inflammation by activating large numbers of T cells. However, Streptococcal pyogenic exotoxin B (SpeB) is an exception, which is pro-inflammatory through its protease activity.
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