Chikungunya Virus Release is Reduced by TIM-1 Receptors Through Binding of Envelope Phosphatidylserine.

Autor:	Ballista JMR; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Hoover AJ; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Noble JT; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Acciani MD; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Miazgowicz KL; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Harrison SA; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Tabscott GAL; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Duncan A; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Barnes DN; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Jimenez AR; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA., Brindley MA; Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA, USA.; Department of Population Health, College of Veterinary Medicine, University of Georgia, Athens, GA, USA.
Jazyk:	angličtina
Zdroj:	BioRxiv : the preprint server for biology [bioRxiv] 2024 Jan 26. Date of Electronic Publication: 2024 Jan 26.
DOI:	10.1101/2024.01.25.577233
Abstrakt:	T-cell immunoglobin and mucin domain protein-1 (TIM-1) mediates entry of Chikungunya virus (CHIKV) into some mammalian cells through the interaction with envelope phospholipids. While this interaction enhances entry, TIM has been shown to tether newly formed HIV and Ebola virus particles, limiting their efficient release. In this study, we investigate the ability of surface receptors such as TIM-1 to sequester newly budded virions on the surface of infected cells. We established a luminescence reporter system to produce Chikungunya viral particles that integrate nano-luciferase and easily quantify viral particles. We found that TIM-1 on the surface of host cells significantly reduced CHIKV release efficiency in comparison to other entry factors. Removal of cell surface TIM-1 through direct cellular knock-out or altering the cellular lipid distribution enhanced CHIKV release. Over the course of infection, CHIKV was able to counteract the tethering effect by gradually decreasing the surface levels of TIM-1 in a process that appears to be mediated by the nonstructural protein 2. This study highlights the importance of phosphatidylserine receptors in mediating not only the entry of CHIKV but also its release and could aid in developing cell lines capable of enhanced vaccine production.
Databáze:	MEDLINE
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