| Polydnavirus | |
|---|---|
| Virus classification | |
| Group: | Group I (dsDNA) |
| Family: | Polydnaviridae |
| Genera | |
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Ichnovirus |
|
The Polydnaviruses ( /pɒˈlɪdnəvaɪərəs/), (PDV) are a family of insect viruses that contain two genera: Ichnoviruses (IV) and Bracoviruses (BV). The ichnoviruses occur in ichneumonid wasps species and bracoviruses in braconid wasps. The genome of the virus is composed of multiple segments of double-stranded, superhelical DNA packaged in capsid proteins and a double layer (IV) or single layer (BV) envelope. Little or no sequence homology exists between BV and IV, suggesting that the two genera evolved independently.
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These viruses are part of a unique biological system consisting of an endoparasitic wasp (parasitoid), an insect (usually lepidopteran) larva, and the virus. The full genome of the virus is integrated into the genome of the wasp and the virus only replicates in specific cells in the female wasp's reproductive system. The virus is injected along with the wasp egg into the body cavity of a lepidopteran host caterpillar and infects cells of the caterpillar. The infection does not lead to replication of new viruses, rather it affects the caterpillar's immune system. Without the virus infection, phagocytic hemocytes (blood cells) will encapsulate and kill the wasp egg but the immune suppression caused by the virus allows for survival of the wasp egg, leading to hatching and complete development of the immature wasp in the caterpillar. Additionally, genes expressed from the polydnavirus in the parasitised host alter host development and metabolism to be beneficial for the growth and survival of the parasitoid larva. Thus the virus and wasp have a symbiotic (mutualistic) relationship.
Both genera of PDV share certain characteristics:
However, the morphology of the two genera are different when observed by electron microscopy. Ichnoviruses tend to be ovoid (egg-shaped) while bracoviruses are short rods.
Nucleic acid analysis suggests a very long association of the viruses with the wasps (greater than 70 million years).
Two proposals have been advanced for how the wasp/virus association developed. The first suggests that the virus is derived from wasp genes. Many parasitoids that do not use PDVs inject proteins that provide many of the same functions, that is, a suppression of the immune response to the parasite egg. In this model, the braconid and ichneumonid wasps packaged genes for these functions into the viruses – essentially creating a gene-transfer system that results in the caterpillar producing the immune-suppressing factors. In this scenario, the PDV structural proteins (capsids) were probably "borrowed" from existing viruses.
The alternative proposal suggests that ancestral wasps developed a beneficial association with an existing virus that eventually led to the integration of the virus into the wasp’s genome. Following integration, the genes responsible for virus replication and the capsids were (eventually) no longer included in the PDV genome. This hypothesis is supported by the distinct morphology differences between IV and BV, suggesting different ancestral viruses for the two families. The IV have remarkable similarities to ascoviruses while BV may be related to baculoviruses
The family Polydnaviridae may have evolved from the Ascoviridae.[1]
An insect's immunity is composed of several mechanisms and all of them can be triggered in the host when the wasp lays its eggs, and during the larvae development.
When a big body (wasp eggs or experimentally, small particles) is introduced into an insect's body, the classic immune reaction is the encapsulation by the hematocytes. An encapsuled body can also be melanised in order to asphyxiate it, thanks to another type of hemocyte, which uses the Phenoloxydase enzyme to produce melanin. Little particles can be phagocyted, and macrophage cells can then be also melanised in a nodule. Finally, insects can also have a humoral immunity, with production of antiviral peptids.(1)
PolyDNAvirus protect the Hymenoptera larvae from the host immune system, acting at different levels.
* First they can disable or destroy hematocytes. The polyDNAvirus associated with Cotesia rubecula, code for un protein CrV1 that desorganise actin filaments in hematocytes, so those cells become less able to move and adher to the larvae (1). Microplitis demolitor Bracovirus (MdBV) induce apoptosis of hematocytes, thanks to its gene PTP-H2 (1). It also decreases hematocytes' capacity of adhesion, thanks to its gene Glc1.8. The gene also decrease phagocytosis.(2)
* PolyDNAvirus can also act on melanisation, MdBV interfer with the production of Phenoloxydase Enzyme.(3)
* Finally, polyDNAvirus can also produce viral Ankyris, that interfere with production of antiviral peptids.(4) Some Ichnovirus, Vankyrin can also prevent apoptosis, the extrem reaction of a cell to block viral propagation.(5)[2]
Another strategy used by parasitoïd Hymenoptera to protect their offspring is production of Virus Like Particles. VLPs are very close to viruses in their structure but they don't carry any nucleic acid. For example, Venturia canescens (Ichneumonidea) and Leptopilina sp. (Figitidaea) produc VLPs.
VLPs can be compared to PolyDNAvirus because they are secreted in the same way, and they both act to protect the larvae against the host's immune system. V. canescens-VLPs (VcVLP1, VcVLP2,VcNEP …) are produced in the calix cells before they go to the oviducts. But they are composed of proteins that are closer in structure and function to Hymenoptera's proteins than to viral proteins. This suggests that they don't have a viral origin, unlike polyDNAvirus.
VLPs protect the Hymenoptera larvae locally, whereas polyDNAvirus can have a more global effect. VLPs allow the larvae to escape the immune system: the larva is not recognised as harmful by its host, or the immune cells can't interact with it thanks to the VLPs.(6)
The wasp Leptopilina heterotoma secrete VLPs that are able to penetrate into the Lamellocytes, thanks to specific receptors, and then modify their shape and surface properties so they become inefficient and the larvae is safe from encapsulation.(7)
MicroRNA are small RNA produced in the host cells thanks to a specific enzymatic machinery. They allows viral RNA destruction. MicroRNA hang on viral-RNA because they are complementary. Then the complex is recognised by an enzyme that destroys it. This phenomenon is known as PTGS (for post transcriptional gene silencing)(8)
It is interesting to consider the microRNA phenomenon in the polyDNAvirus context. Lots of hypotheses can be formulated :