the parasite insect and causes significant physiological and developmental alterations in the parasite's host. The segmented polydnavirus genome consists of double-stranded superhelical molecules; each segment is apparently integrated into the chromosomal DNA of each male and female wasp. The virus replicates in the nucleus of calyx cells and is secreted into the oviduct. When the virus is transferred to the host insect during oviposition, gene expression induces host immunosuppression and developmental arrest, which ensures successful development of the immature endoparasite. In the host, polydnavirus expression is detected by 2 hr and during endoparasite development. Most of the abundantly expressed viral genes expressed very early after parasitization belong to multigene families. Among these families, the "cysteine-rich" gene family is the most studied, and it may be important in inducing host manifestations resulting in parasite survival. This gene family is characterized by a similar gene structure with introns at comparable positions within the 5' untranslated sequence and just 5' to a specific cysteine codon (*C) within a cysteine motif, C-*C-CC-C-C. Another unusual feature is that the nucleotide sequences of introns 2 in the subfamily WHv1.0/WHv1.6 are more conserved than those of the flanking exons. The structures of these viral genes and possible functions for their encoded protein are considered within the context of the endoparasite and virus strategy for genetic adaptation and successful parasitization.

We thank Brent Graham, Sharon Braunagel, and Shelley Bennett for their critical evaluation of this paper. This study was funded in part by National Science Foundation Grant IBN-9119827 and Texas Agricultural Experiment Station Project 8078.

REFERENCES

1. Stoltz, D. B. & Vinson, S. B. (1979) Adv. Virus Res. 24, 125-171.

2. Stoltz, D. B. (1993) in Parasites and Pathogens of Insects, eds. Beckage, N. E., Thompson, S. M. & Federici, B. A. (Academic, San Diego ) Vol. 1, pp. 167-187.

3. Fleming, J. G. W. & Summers, M. D. (1986) J. Virol. 57, 552-562.

4. Fleming, J. G. W. & Summers, M. D. (1991) Proc. Natl. Acad. Sci. USA 88, 9770-9774.

5. Fleming, J. G. W. (1991) Biol. Control 1, 127-135.

6. Fleming, J. G. W. & Krell, P. J. (1993) in Parasites and Pathogens of Insects, eds. Beckage, N. E., Thompson, S. M. & Federici, B. A. (Academic, San Diego), Vol. 1, pp. 189-225.

7. Webb, B. A. & Summers, M. D. (1992) Experientia 48, 1018-1022.

8. Beckage, N. E. (1993) in Parasites and Pathogens of Insects, eds. Beckage, N. E., Thompson, S. M. & Federici, B. A. (Academic, San Diego), Vol. 1, pp. 25-57.

9. Beckage, N. E. (1993) Receptor 3, 233-245.

10. Thompson, S. N. (1993) in Parasites and Pathogens of Insects, eds. Beckage, N. E., Thompson, S. M. & Federici, B. A. (Academic, San Diego), Vol. 1, pp. 125-144.



The National Academies | 500 Fifth St. N.W. | Washington, D.C. 20001
Copyright © National Academy of Sciences. All rights reserved.
Terms of Use and Privacy Statement