Parasitization of Manduca sexta larvae by the parasitoid wasp Cotesia congregata induces an impaired host immune response

Amaya, Kevin E., Asgari, Sassan, Jung, Richard, Hongskula, Melissa and Beckage, Nancy E. (2005) Parasitization of Manduca sexta larvae by the parasitoid wasp Cotesia congregata induces an impaired host immune response. Journal of Insect Physiology, 51 5: 505-512. doi:10.1016/j.jinsphys.2004.11.019

Author Amaya, Kevin E.
Asgari, Sassan
Jung, Richard
Hongskula, Melissa
Beckage, Nancy E.
Title Parasitization of Manduca sexta larvae by the parasitoid wasp Cotesia congregata induces an impaired host immune response
Journal name Journal of Insect Physiology   Check publisher's open access policy
ISSN 0022-1910
Publication date 2005-05-01
Year available 2005
Sub-type Article (original research)
DOI 10.1016/j.jinsphys.2004.11.019
Open Access Status DOI
Volume 51
Issue 5
Start page 505
End page 512
Total pages 8
Editor D.L. Denlinger
S.E. Reynolds
Place of publication Oxford
Publisher Pergamon Press
Language eng
Subject C1
270303 Virology
780105 Biological sciences
Abstract During oviposition, the parasitoid wasp Cotesia congregata injects polydnavirus, venom, and parasitoid eggs into larvae of its lepidopteran host.. the tobacco hornworm, Manduca sexta. Polydnaviruses (PDVs) suppress the immune system of the host and allow the juvenile parasitoids to develop without being encapsulated by host hemocytes mobilized by the immune system. Previous work identified a gene in the Cotesia rubecula PDV (CrV1) that is responsible for depolymerization of actin in hemocytes of the host Pieris rapae during a narrow temporal window from 4 to 8 h post-parasitization. Its expression appears temporally correlated with hemocyte dysfunction. After this time, the hemocytes recover, and encapsulation is then inhibited by other mechanism(s). In contrast, in parasitized tobacco hornworm larvae this type of inactivation in hemocytes of parasitized M. sexta larvae leads to irreversible cellular disruption. We have characterized the temporal pattern of expression of the CrV1-homolog from the C. congregata PDV in host fat body and hemocytes using Northern blots, and localized the protein in host hemocytes with polyclonal antibodies to CrV1 protein produced in P. rapae in response to expression of the CrV1 protein. Host hemocytes stained with FITC-labeled phalloidin, which binds to filamentous actin, were used to observe hemocyte disruption in parasitized and virus-injected hosts and a comparison was made to hemocytes of nonparasitized control larvae. At 24 h post-parasitization host hemocytes were significantly altered compared to those of nonparasitized larvae. Hemocytes front newly parasitized hosts displayed blebbing, inhibition of spreading and adhesion, and overall cell disruption. A CrV1-homolog gene product was localized in host hemocytes using polyclonal CrV1 antibodies, suggesting that CrV1-like gene products of C. congregata's bracovirus are responsible for the impaired immune response of the host. (C) 2005 Elsevier Ltd. All rights reserved.
Keyword Entomology
Insect Immunity
Tobacco Hornworm
Braconid Wasp
Host Immunosuppression
Lacanobia-oleracea Lepidoptera
Polydnavirus Sequences
Q-Index Code C1
Institutional Status UQ
Additional Notes DOI: 10.1016/j.jinsphys.2004.11.019

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Created: Wed, 15 Aug 2007, 15:21:05 EST