Chen, Yan PingPettis, Jeffery SCorona, MiguelChen, Wei PingLi, Cong JunSpivak, MarlaVisscher, P. KirkDeGrandi-Hoffman, GloriaBoncristiani, HumbertoZhao, YanvanEngelsdorp, DennisDelaplane, KeithSolter, LeellenDrummond, FrancisKramer, MatthewLipkin, W. IanPalacios, GustavoHamilton, Michele CSmith, BartonHuang, Shao KangZheng, Huo QingLi, Ji LianZhang, XuanZhou, Ai FenWu, Li YouZhou, Ji ZhongLee, Myeong-LTeixeira, Erica WLi, Zhi GuoEvans, Jay DSchneider, David S2016-07-062016-07-062014Chen, Yan Ping, Pettis, Jeffery S, Corona, Miguel, Chen, Wei Ping, Li, Cong Jun, Spivak, Marla, . . . Schneider, David S. (2014). Israeli Acute Paralysis Virus: Epidemiology, Pathogenesis and Implications for Honey Bee Health (The Epidemiology and Pathogenesis of Israeli Acute Paralysis Virus). 10(7), E1004261.https://hdl.handle.net/11299/181255Israeli acute paralysis virus (IAPV) is a widespread RNA virus of honey bees that has been linked with colony losses. Here we describe the transmission, prevalence, and genetic traits of this virus, along with host transcriptional responses to infections. Further, we present RNAi-based strategies for limiting an important mechanism used by IAPV to subvert host defenses. Our study shows that IAPV is established as a persistent infection in honey bee populations, likely enabled by both horizontal and vertical transmission pathways. The phenotypic differences in pathology among different strains of IAPV found globally may be due to high levels of standing genetic variation. Microarray profiles of host responses to IAPV infection revealed that mitochondrial function is the most significantly affected biological process, suggesting that viral infection causes significant disturbance in energy-related host processes. The expression of genes involved in immune pathways in adult bees indicates that IAPV infection triggers active immune responses. The evidence that silencing an IAPV-encoded putative suppressor of RNAi reduces IAPV replication suggests a functional assignment for a particular genomic region of IAPV and closely related viruses from the Family Dicistroviridae, and indicates a novel therapeutic strategy for limiting multiple honey bee viruses simultaneously and reducing colony losses due to viral diseases. We believe that the knowledge and insights gained from this study will provide a new platform for continuing studies of the IAPV–host interactions and have positive implications for disease management that will lead to mitigation of escalating honey bee colony losses worldwide.enArticle10.1371/journal.ppat.1004261