respiratory syncytial virus assembles into structured filamentous virion particles independently of host cytoskeleton and related proteins呼吸道合胞体病毒结构组装成丝状病毒粒子粒子独立于宿主细胞骨架和相关蛋白质.pdfVIP

respiratory syncytial virus assembles into structured filamentous virion particles independently of host cytoskeleton and related proteins呼吸道合胞体病毒结构组装成丝状病毒粒子粒子独立于宿主细胞骨架和相关蛋白质.pdf

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respiratory syncytial virus assembles into structured filamentous virion particles independently of host cytoskeleton and related proteins呼吸道合胞体病毒结构组装成丝状病毒粒子粒子独立于宿主细胞骨架和相关蛋白质

Respiratory Syncytial Virus Assembles into Structured Filamentous Virion Particles Independently of Host Cytoskeleton and Related Proteins 1 1 1 4 3 Fyza Y. Shaikh , Thomas J. Utley , Ryan E. Craven , Meredith C. Rogers , Lynne A. Lapierre , James R. Goldenring3, James E. Crowe, Jr.1,2,5* 1 Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 2 Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 3 Department of Surgery and the Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 4 The Medical Scientist Training Program, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America, 5 The Vanderbilt Vaccine Center, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America Abstract Respiratory syncytial virus (RSV) is a single-stranded RNA virus that assembles into viral filaments at the cell surface. Virus assembly often depends on the ability of a virus to use host proteins to accomplish viral tasks. Since the fusion protein cytoplasmic tail (FCT) is critical for viral filamentous assembly, we hypothesized that host proteins important for viral assembly may be recruited by the FCT. Using a yeast two-hybrid screen, we found that filamin A interacted with FCT, and mammalian cell experiments showed it localized to viral filaments but did not affect viral replication. Furthermore, we found that a number of actin-associated proteins also were excluded from viral filaments. Actin or tubulin cytoskeletal rearrangement was not

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