ATP synthesis is active on the cell surface of the shrimp Litopenaeus vannamei and is suppressed by WSSV infection
- PDF / 3,924,376 Bytes
- 10 Pages / 595.276 x 793.701 pts Page_size
- 45 Downloads / 172 Views
RESEARCH
Open Access
ATP synthesis is active on the cell surface of the shrimp Litopenaeus vannamei and is suppressed by WSSV infection Yan Liang, Meng-Lin Xu, Xiao-Wen Wang, Xiao-Xiao Gao, Jun-Jun Cheng, Chen Li and Jie Huang*
Abstract Background: Over the past a few years, evidences indicate that adenosine triphosphate (ATP) is an energy source for the binding, maturation, assembly, and budding process of many enveloped viruses. Our previous studies suggest that the F1-ATP synthase beta subunit (ATPsyn β, BP53) of the shrimp Litopenaeus vannamei (L. vannamei) might serve as a potential receptor for white spot syndrome virus (WSSV)’s infection. Methods: BP53 was localized on the surface of shrimp hemocytes and gill epithelial cells by immunofluorescence assay and immunogold labeling technique. Cell surface ATP synthesis was demonstrated by an in vitro bioluminescent luciferase assay. Furthermore, the expression of bp53 after WSSV infection was investigated by RT-PCR test. In addition, RNAi was developed to knock down endogenous bp53. Results: BP53 is present on shrimp cell surface of hemocytes and gill epithelia. The synthesized ATP was detectable in the extracellular supernatant by using a bioluminescence assay, and the production declined post WSSV binding and infection. Knocking down endogenous bp53 resulted in a 50% mortality of L. vannamei. Conclusion: These results suggested that BP53, presenting on cell surface, likely served as one of the receptors for WSSV infection in shrimp. Correspondingly, WSSV appears to disturb the host energy metabolism through interacting with host ATPsyn β during infection. This work firstly showed that host ATP production is required and consumed by the WSSV for binding and proceeds with infection process. Keywords: White spot syndrome virus, Shrimp, F1-ATP synthase beta subunit, Cell surface ATP synthesis, Virus binding, RNAi, Receptor
Introduction White spot syndrome virus (WSSV), the only member of the genus Whispovirus of the family of Nimaviridae, has emerged globally as one of the most prevalent and lethal pathogen for Penaeid shrimp species since its first outbreak in 1992 [1]. The better understanding of its pathogenesis, especially the nature of virus–host interactions, will eventually lead to the development of new strategies to control white spot viral disease. It is well known that attachment/binding to the host cell surface is essential for initiation of a viral infection [2]. This virus–host interactions may also trigger a serial host * Correspondence: [email protected] Key Laboratory of Sustainable Development of Marine Fisheries, Ministry of Agriculture, Yellow Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, No.106 Nanjing Road, Qingdao 266071, China
immune responses against the invader as well as some modifications of host gene expression to facilitate virus replication [3]. Recently several WSSV envelope proteins [VP37 (VP281), VP28, VP187, and VP53A], and some cellular proteins of shrimp [PmRab7, β-integrin, PmCBP, and F1-ATP syn
Data Loading...
