A myeloid differentiation-like protein in partnership with Toll5 from the pest insect Spodoptera litura senses baculovirus infection

成果类型:
Article
署名作者:
Zhang, Ruonan; Zhong, Jielai; Li, Yanjun; Li, Mengge; Zhang, Jie; Hu, Qihao; Wen, Liang; Xu, Xiaoxia; Jin, Fengliang; Yang, Wanying; Lu, Yuzhen; Strand, Michael R.; Yu, Xiao-Qiang
署名单位:
South China Normal University; South China Agricultural University; South China Agricultural University; University System of Georgia; University of Georgia
刊物名称:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
ISSN/ISSBN:
0027-9968
DOI:
10.1073/pnas.2415398121
发表日期:
2024-10-29
关键词:
nuclear polyhedrosis-virus californica m-nucleopolyhedrovirus rna interference innate immunity drosophila RECOGNITION PATHWAY autophagy gene activation
摘要:
Many types of viruses infect insects and other arthropods. In contrast, little is known about how arthropods sense viruses, although several innate immune pathways including Toll have antiviral functions. Large DNA viruses in the family Baculoviridae are used to control a number of pest insects. Here, we studied Spodoptera litura and Autographa californica multiple nucleopolyhedrovirus (AcMNPV) to test the hypothesis that one or more myeloid differentiation-like (ML) proteins and Toll family members sense baculoviruses. We identified 11 ML and 12 Toll genes in the S. litura genome. A series of experiments indicated that S. litura ML protein 11 (SlML-11) binds the budded form of AcMNPV and partners with S. litura Toll5 (SlToll5). SlML-11 also bound sphingomyelin (SPM), which is a component of the virion envelope. Disabling SlML-11 and SlToll5 increased susceptibility to infection, while priming larvae with SPM reduced susceptibility as measured by increased survival to the adult stage and clearance of AcMNPV from individuals that emerged as adults. We conclude that SPM is a pathogen- associated molecular pattern molecule while SlML-11 and SlToll5 interact to function as a pattern recognition receptor that senses AcMNPV.