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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Actin Cytoskeleton, Actin Depolymerizing Factors, Animals, Caveolin 1, Cell Line, Cell Membrane, Cholesterol, Cricetinae, Dynamin II, Encephalitis Virus, Japanese, Encephalitis, Japanese, Endocytosis, ErbB Receptors, HEK293 Cells, Host-Pathogen Interactions, Humans, Life Cycle Stages, Membrane Transport Proteins, Neurons, Phosphatidylinositol 3-Kinases, Phosphorylation, Protein-Tyrosine Kinases, RNA, Small Interfering, Signal Transduction, Transfection, Virus Attachment, Virus Internalization, rac1 GTP-Binding Protein, rhoA GTP-Binding Protein.
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Does caveolin-1-mediated Japanese encephalitis virus entry require a two-step regulation of actin reorganization? Context: To investigate the detailed mechanism of Japanese encephalitis virus (JEV) cell entry. Utilize a siRNA library targeting cellular membrane trafficking genes to identify key molecules that mediate JEV entry into human neuronal cells. JEV enters human neuronal cells by caveolin-1-mediated endocytosis, which depends on a two-step regulation of actin cytoskeleton remodeling triggered by RhoA and Rac1: RhoA activation promoted the phosphorylation of caveolin-1, and then Rac1 activation facilitated caveolin-associated viral internalization. Specifically, virus attachment activates the EGFR-PI3K signaling pathway, thereby leading to RhoA activation.
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This work provides a detailed picture of the entry route and intricate cellular events following the entry of JEV into human neuronal cells, and promotes a better understanding of JEV entry. Final Decision: yes