532 Boman and Hultmark (1987) compared the immune mechanisms of insects and ver tebrates. They noted that insects have relatively good physical protection from potential invaders by way of the cuticle and peritrophic matrix, whereas vertebrates offer greater access viathe mucous linings of the digestive, respiratory, excretory, and reproductive systems. The link between the duration of an immune response and the life span and reproductive rate was also considered. Thus, in insects, with generally short lives but high fecundity, the immune response is very rapid, being based on RNA and protein synthesis, and is broad spectrum in nature. In contrast, in vertebrates, which have a long life span and produce relatively few offspring, the immune response is based on cell proliferation and is much longer lasting and highly specific. Of course, there are exceptions to every rule, and it is interesting that work on Periplaneta americana, which for an insect is relatively long-lived, indicates the existence in this species of a specific, long-lived "memory" type of immune response, functionally similar to that of vertebrates (Dunn, 1986, 1990).

Finally, it should be noted that the development of an immune response is not without costs to the host. The costs include not only those associated with developing and maintaining the potential for an immune response, but also longer-term responses. For example, successful defense against parasitoid attack by larvae of Drosophila leads to a reduction in adult size and number of eggs produced, as well as greater susceptibility to pupal parasitoids. Further, larvae whose immune system has been challenged have reduced competitive ability when food is limited, compared to unchallenged larvae (Kraaijeveld et al., 2002).

5.2.1. Resistance to Host Immunity

Though humans have not solved the mystery of how hemocytes recognize foreign matter, many parasites and pathogens obviously have because on entering a host they do not elicit a reaction, with disastrous consequences for the host. Boman and Hultmark (1987) distinguished between passive and active resistance to host immunity.

In passive resistance the pathogen's or parasite's mechanism for avoiding attack is already in place on entry into the host. For example, many parasitic Hymenoptera oviposit with great precision in specific tissues of the host so that the egg does not trigger the immune response. Similarly, some nematodes, on entering the insect's body, immediately migrate to a ganglion where they grow rapidly and undisturbed (Vinson, 1990). Several mechanisms are used to prevent an encapsulation response. For example, the eggs of some parasitoids are coated with material that prevents hemocytes from sticking to them (Eslin and Prevost, 2000). Another tactic is for the eggs to be covered by a fibrous coat that is not recognized as foreign (Hu et al., 2003). In a slight variation on this theme, the eggs and larvae of the ichneumonid wasp Venturia (= Nemeritis) canescens are covered by a glycoprotein layer that binds the host's plasma lipophorin, which thereby camouflages the foreign egg surface (Kinuthia etal., 1999).

Active resistance refers to active steps taken by the invader when the host's system attempts to attack it. One strategy is for the parasitoid to deposit its eggs before the host's immune system is very responsive. For example, the braconid wasp Asobara tabida preferentially oviposits in first- or second-instar larvae of Drosophila in which there are few circulating hemocytes. Growth of the parasitoid larva is very rapid, which further reduces the likelihood of efficient encapsulation. Other active resistance mechanisms include the introduction into the host, at the time of egg deposition, of (1) compounds that suppress production of humoral immunogens such as the antibacterial peptides, (2) substances that degrade or inhibit activity of the immunogens, or (3) chemicals that inhibit mobilization or multiplication of hemocytes. For example, the parasitic nematode Heterorhabditis bacterio- 533

phora releases a proteinase that specifically degrades cecropins in the wax moth Galleria mellonella (Jarosz, 1998). However, the majority of evidence for these mechanisms has lys°em come from studies on hymenopteran parasitoids.

Except in some braconids and ichneumonids (see below), hymenopteran venom, produced by the female accessory glands (Figure 19.1) and injected at oviposition, may attack host granulocytes, causing them to lyse or lose their ability to spread over a foreign surface. The venom also interferes with the host's endocrine and metabolic systems. As a result of the disruption to its hormone levels, the host can no longer molt, though it continues to feed. The venom also interferes with the normal process of storage of nutrient reserves by the fat body. Collectively, these two effects enable the parasitoid larva to grow and mature rapidly in a food-rich environment, without the risk that the host will metamorphose prematurely (Vinson, 1990; Coudron, 1991; Strand andPech, 1995).

Some braconid and ichneumonid wasps, on the other hand, have entered into a remarkable symbiosis with a virus as their strategy for resisting host attack. As these wasps oviposit, they inject a protein together with numerous particles of polydnavirus, so-called because these complex viruses have up to 28 complete double-stranded circles of DNA (Beckage, 1997; Shelby and Webb, 1999). The ovarian protein temporarily blocks encapsulation by causing the granulocytes and plasmatocytes to lyse, giving the polydnavirus time to invade the host's tissues where viral protein synthesis begins. By about 24 hours after oviposition, when the ovarian protein is no longer effective, sufficient viral protein has been produced that lysis of hemocytes continues and encapsulation does not occur. The polydnavirus also has two other major effects on the host's immune response. It inhibits the prophenoloxidase cascade, preventing production of melanin and quinones, and it significantly reduces the production and release of antibacterial peptides in the fat body. Like venom, polydnavirus also inhibit the host's normal development and metabolism. Specifically, synthesis of molting hormone and juvenile hormone esterase are inhibited, while production of juvenile hormone is enhanced. Collectively these actions prevent the host from growing and molting normally (see Chapter 21, Section 6.1). Simultaneously, the virus disrupts the synthesis of storage hexamers and carbohydrates, presumably allowing the parasitoid easier access to nutrients. It should be stressed that production of viral particles occurs only in the female parasitoid, specifically in the calyx region of the reproductive tract (Figure 19.1). Curiously, however, the polydnavirus genome is part of the genome of both male and female wasps. Further, some polydnavirus genes are identical to those that code for venom proteins, raising the fascinating question of whether the polydnavirus had an independent evolutionary origin or has always been an integral part of the wasp's genome (Beckage, 1997).

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