Role of Ovarian Proteins Secreted by Toxoneuron nigriceps (Viereck) (Hymenoptera, Braconidae) in the Early Suppression of Host Immune Response

Insects

Paola Varricchio¹  Annalisa Grimaldi²  S. Bradleigh Vinson³  Rosanna Salvia⁴  Patrizia Falabella⁴  Paolo Fanti⁴  Antonio Moretta⁴  Antonio Franco⁴  Carmen Scieuzo⁴ 

[1] Department of Agricultural Sciences, University of Naples “Federico II”, 80055 Portici, Italy;Department of Biotechnology and Life Science, University of Insubria, Via J.H. Dunant 3, 21100 Varese, Italy;Department of Entomology, Texas A&M University, 370 Olsen Blvd, College Station, TX 77843-2475, USA;Department of Sciences, University of Basilicata, Via dell’Ateneo Lucano 10, 85100 Potenza, Italy;

关键词: Ovarian Proteins;    host-parasitoid interaction;    Heliothis virescens;    Toxoneuron nigriceps;   

DOI  :  10.3390/insects12010033

来源: DOAJ

【 摘 要 】

Toxoneuron nigriceps (Viereck) (Hymenoptera, Braconidae) is an endophagous parasitoid of the larval stages of the tobacco budworm, Heliothis virescens (Fabricius) (Lepidoptera, Noctuidae). During oviposition, T. nigriceps injects into the host body, along with the egg, the venom, the calyx fluid, which contains a Polydnavirus (T. nigriceps BracoVirus: TnBV), and the Ovarian Proteins (OPs). Although viral gene expression in the host reaches detectable levels after a few hours, a precocious disruption of the host metabolism and immune system is observed right after parasitization. This alteration appears to be induced by female secretions including TnBV venom and OPs. OPs, originating from the ovarian calyx cells, are involved in the induction of precocious symptoms in the host immune system alteration. It is known that OPs in braconid and ichneumonid wasps can interfere with the cellular immune response before Polydnavirus infects and expresses its genes in the host tissues. Here we show that T. nigriceps OPs induce several alterations on host haemocytes that trigger cell death. The OP injection induces an extensive oxidative stress and a disorganization of actin cytoskeleton and these alterations can explain the high-level of haemocyte mortality, the loss of haemocyte functionality, and so the reduction in encapsulation ability by the host.

【 授权许可】

Unknown