Polydnavirus infection inhibits synthesis of an insect plasma protein, arylphorin

Abstract

The wasp Campoletis sonorensis injects a segmented, double-stranded DNA polydnavirus (CsPDV) along with its egg during parasitization of Heliothis virescens larvae. After parasitization, CsPDV protects the wasp egg and larva by selectively disabling the host's cellular immune response. Other host physiological systems including growth and development are affected to the apparent benefit of the parasite. To begin the characterization of the biochemical effects and mode of action of CsPDV on host growth, the titre of a developmentally regulated insect storage protein, arylphorin, was studied. Parasitized or virus-infected insects had substantially less circulating arylphorin than control insects. Fat bodies from parasitized larvae also synthesized less arylphorin in vitro. However, Northern blots of total RNA from parasitized and non-parasitized, control insects showed that the arylphorin transcript level was unaffected by parasitization suggesting a biochemical block at the translational level. In vitro translation followed by immunoprecipitation ofarylphorin indicated that the mRNA was present and translatable at equal levels in both parasitized and control insects. Injection of purified virus elicited the response observed in naturally parasitized larvae, demonstrating that the effect on arylphorin synthesis is mediated, either directly or indirectly, by polydnavirus gene product(s).

Isolation and characterization of a member of the cysteine-rich gene family from Campoletis sonorensis polydnavirus

“…During oviposition, polydnavirus, venom, and ovarian proteins are injected together with the wasp eggs into H. virescens larvae. It has been shown that introduction of CsPDV alone into H. virescens larvae causes dramatic physiological changes that mimic natural parasitization (Edson et al, 1981;Shelby & Webb, 1994). However, recent studies demonstrate that an ovarian protein complex rapidly but transiently inactivates the H. virescens encapsulation response early in parasitization (Webb & Luckhart, 1994.…”

Expression of polydnavirus genes under polydnavirus promoter regulation in insect larvae infected with baculovirus recombinants

“…Alterations in the physiology of the lepidopteran host are required for survival and development of the wasp endoparasite. The titres of many developmentally regulated hormones and proteins may be affected by polydnavirus infection (Fathpour & Dahlman, 1995;Shelby & Webb, 1994) but it is not clear which, if any, of these alterations are primary effects of virus infection and which changes are secondary effects resulting from virusassociated alteration of the host's developmental programme. Clearly, the identification of viral genes responsible for the disruption of host physiology and the elucidation of the mechanisms through which physiological systems are targeted by viral genes is a principal objective in the study of polydnaviruses.…”

“…Parasitized insects display an array of physiological symptoms that include alterations in growth, Author for correspondence: Bruce Webb. Fax + 1 606 323 1120. e-mail bawebb@pop.uky.edu development, immunity, blood protein composition, blood amino acid titres and behaviour (Fathpour & Dahlman, 1995;Shelby & Webb, 1994;Strand & Pech, 1995;Summers & DibHajj, 1995). Importantly, polydnavirus effects are not associated with virus replication but rather with the species-specific regulation of virus gene expression.…”

Iκβ-Related vankyrin Genes in the Campoletis sonorensis Ichnovirus: Temporal and Tissue-Specific Patterns of Expression in Parasitized Heliothis virescens Lepidopteran Hosts

“…Heliothis virescens larvae causes severe physiological changes in the host, including developmental arrest, a suppression of cellular and humoral immunity, and a decrease in host growth-associated hemolymph proteins such as arylphorin (13,41,62,63,64,66,85). Increased susceptibility to pathogenic attack has been partly attributed to decreased induction of cecropin and lysozyme activities in hosts of C. sonorensis (65).…”

“…Virions are then transferred to the parasitoid's lepidopteran hosts with eggs, ovarian proteins, and venom during parasitization, where they infect local tissues, express encoded genes, and induce pathologies essential to the survival of the developing endoparasite (38,64,70,75,81,84). These pathological alterations include disruption of host development, immunosuppression, and mobilization of host protein stores for parasitoid utilization (2,3,13,17,30,41,50,62,64,66,74,85).…”