alter haemocyte function. Viral transcripts are expressed in some host–
parasite systems at near steady-state levels beginning a few hours after
wasp oviposition and continuing until the wasp’s progeny complete
development (Theilmann and Summers, 1986; Strandet al., 1992). In
other systems, viral expression is transient, lasting less than 36 h after
wasp oviposition (Harwoodet al., 1994; Asgariet al., 1996; Strandet al.,
1997). Other viral and microbial symbionts besides polydnaviruses have
also been reported in other groups of parasitoids, but these remain poorly
characterized (Quicke, 1997).
Other factors potentially involved in overcoming host defences are
teratocytes and the parasitoid larva itself. Teratocytes are derived from the
serosal membrane that surrounds the embryos of hymenopteran para-
sitoids in the families Braconidae and Scelionidae. From 30 to more than
800 teratocytes per parasitoid are released into the host’s haemocoel,
where they continue to grow but not divide. Several studies implicate
teratocytes in altering both host development and encapsulation
(reviewed by Vinson and Iwantsch, 1980; Strand, 1986; Dahlman, 1990).
The molecular bases for these effects are unclear, although recent studies
suggest that teratocytes from the braconidMicroplitis croceipessecrete
a protein that disrupts host protein synthesis (B.A. Webb, personal
communication). Endoparasitoid larvae also secrete factors that have been
implicated in disrupting encapsulation and host development (Fuhrer
and Willers, 1986; Brown and Reed-Larson, 1991).Parasitoid-induced Changes in Host Development
As previously noted, the hosts of idiobionts cease to develop after
parasitism, while the hosts of koinobionts continue to grow. Hosts para-
sitized by ectoparasitoids usually cease to develop, because adults inject
paralysing venoms (Piek, 1986). After hatching, ectoparasitoid larvae and
egg parasitoids secrete enzymes while feeding that extraorally digest host
tissues and, in the process, accelerate host death (Strand, 1986). The
developmental interactions between koinobiont larvae and their hosts, in
contrast, are more complex. As a general rule, hosts parasitized by solitary
endoparasitoids usually grow more slowly and attain smaller sizes
than non-parasitized individuals, whereas hosts parasitized by gregarious
endoparasitoids attain sizes only modestly smaller or sometimes actually
larger than non-parasitized hosts. Hosts parasitized by larval endo-
parasitoids are also usually unable to initiate metamorphosis.
These changes in host development are due in part to alterations
in endocrine physiology. The growth and metamorphosis of insects are
controlled primarily by the interplay between ecdysteroids released by
the prothoracic glands, which induce an insect to moult, and juvenile
hormone (JH) from the corpora allata, which controls the type of moult an
insect undergoes (Riddiford, 1985; Nijhout, 1994). A high JH titre during
ecdysteroid release results in moulting to another larval or nymphal stage,138 M.R. Strand