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Persistent Rhesus Enteric Calicivirus Infection in Recombinant CHO Cells Expressing the Coxsackie and Adenovirus Receptor.
Viruses
November 2024
Department of Veterinary Pathobiology, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University, College Station, TX 77843, USA.
Recently, using a panel of recombinant CHO cell lines, we identified the coxsackie and adenovirus receptor (CAR) and histo-blood group antigens (HBGAs) or sialic acid as the minimum requirement for susceptibility to rhesus enteric calicivirus (ReCV) infections. While ReCVs cause lytic infection in LLC-MK2 cells, recombinant CHO (rCHO) cell lines did not exhibit any morphological changes upon infection. To monitor infectious virus production, rCHO cell cultures had to be freeze-thawed and titrated on LLC-MK2 monolayers.
View Article and Find Full Text PDFLoss-of-Function of CLMP Is Associated With Congenital Short Bowel Syndrome and Impaired Intestinal Development.
Clin Genet
January 2025
Division of Pediatric Gastroenterology and Nutrition, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Coxsackie and adenovirus receptor-like membrane protein (CLMP) mutation is identified as a genetic risk factor of congenital short bowel syndrome (CSBS). However, the specific pathogenic mechanism remains unclear. This study aimed to explore the clinical manifestations, genetic characteristics, and molecular mechanisms underlying CSBS caused by CLMP mutations.
View Article and Find Full Text PDFCoxsackievirus and adenovirus receptor expression facilitates enteroviral infections to drive the development of pancreatic cancer.
Nat Commun
December 2024
Department of Cancer Biology, Mayo Clinic, Jacksonville, FL, 32224, USA.
The development of pancreatic cancer requires both, acquisition of an oncogenic mutation in KRAS as well as an inflammatory insult. However, the physiological causes for pancreatic inflammation are less defined. We show here that oncogenic KRas-expressing pre-neoplastic lesion cells upregulate coxsackievirus (CVB) and adenovirus receptor (CAR).
View Article and Find Full Text PDFCoxsackievirus B3 Activates Macrophages Independently of CAR-Mediated Viral Entry.
Viruses
September 2024
Centre for Heart Lung Innovation, University of British Columbia, St. Paul's Hospital, Vancouver, BC V6Z 1Y6, Canada.
Article Synopsis
- * The study focused on how CVB3 interacts with macrophage cells, revealing that it activates these immune cells without replicating inside them and that macrophages lack the viral entry receptor needed for infection.
- * Additionally, introducing the receptor in macrophages did not enable viral replication but changed inflammatory responses; the research also identified the autophagy protein LC3 as a key player in activating macrophages.
SAR Analysis of Novel Coxsackie virus A9 Capsid Binders.
J Med Chem
October 2024
Department of Drug Chemistry and Technologies, Sapienza University of Rome, 00185 Rome, Italy.
Enterovirus infections are common in humans, yet there are no approved antiviral treatments. In this study we concentrated on inhibition of one of the (EV-B), namely Coxsackievirus A9 (CVA9), using a combination of medicinal chemistry, virus inhibition assays, structure determination from cryogenic electron microscopy and molecular modeling, to determine the structure activity relationships for a promising class of novel -phenylbenzylamines. Of the new 29 compounds synthesized, 10 had half maximal effective concentration (EC) values between 0.
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