Grant sponsor: National Natural Science Foundation of China; Grant numbers: 30770281; 31071977; Grant sponsor: Shandong Provincial Natural Science Foundation, China; Grant number: Y2007D51.
SUPPRESSION OF AcMNPV REPLICATION BY ADF AND THYMOSIN PROTEIN UP-REGULATION IN A NEW TESTIS CELL LINE, Ha-shl-t
Article first published online: 11 JAN 2013
© 2013 Wiley Periodicals, Inc.
Archives of Insect Biochemistry and Physiology
Volume 82, Issue 3, pages 158–171, March 2013
How to Cite
Zhang, X., Chen, M., Ma, X., Zhao, X., Wang, J., Shao, H., Song, Q. and Stanley, D. (2013), SUPPRESSION OF AcMNPV REPLICATION BY ADF AND THYMOSIN PROTEIN UP-REGULATION IN A NEW TESTIS CELL LINE, Ha-shl-t. Arch. Insect Biochem. Physiol., 82: 158–171. doi: 10.1002/arch.21082
- Issue published online: 15 FEB 2013
- Article first published online: 11 JAN 2013
- National Natural Science Foundation of China. Grant Numbers: 30770281, 311071977
- Shandong Provincial Natural Science Foundation, China. Grant Number: Y2007D51
- testis cell line
Host cytoskeletons facilitate the entry, replication, and egress of viruses because cytoskeletons are essential for viral survival. One mechanism of resisting viral infections involves regulating cytoskeletal polymerization/depolymerization. However, the molecular mechanisms of regulating these changes in cytoskeleton to suppress viral replication remain unclear. We established a cell line (named Ha-shl-t) from the pupal testis of Helicoverpa armigera (Lepidoptera: Noctuidae). The new testis cell line suppresses Autographa californica multiple nucleocapsid nucleopolyhedrovirus (AcMNPV) replication via disassembly of cytoskeleton. Up-regulation of thymosin (actin disassembling factor) and adf (actin depolymerizing factor) reduces F-actin. Silencing thymosin or adf or treating cells with the F-actin stabilizer phalloidin led to increased AcMNPV replication, while treating cells with an F-actin assembly inhibitor cytochalasin B decreased viral replication. We infer that Ha-shl-t cells utilize F-actin depolymerization to suppress AcMNPV replication by up-regulating thymosin and adf. We propose Ha-shl-t as a model system for investigating cytoskeletal regulation in antiviral action and testicular biology generally.