Полиднавирусы: симбиоз с наездниками и подавление иммунитета насекомых.

Family of viruses

Polydnaviriformidae (/p//ɒ/'/l//ɪ//d//n//ə//v//ɪ//r//ə//,//f//O://m//ɪ//d//ɛ/ PDV) is a family of insect viriforms; members are known as polydnaviruses. There are two genera in the family: Bracoform and Ichnoviriform. Polydnaviruses form a symbiotic relationship with parasitoid wasps. Ichnoviriforms (IV) occur in Ichneumonid wasps and Bracoviriforms (BV) in Braconid wasps. The larvae of wasps in both of those groups are themselves parasitic on Lepidoptera (moths and butterflies), and the polydnaviruses are important in circumventing the immune response of their parasitized hosts. Little or no sequence homology exists between BV and IV, suggesting that the two genera have been evolving independently for a long time.

Viruses in Polydnaviridae are enveloped, with prolate ellipsoid and cylindrical geometries. Genomes are circular and segmented, composed of multiple segments of double stranded, superhelical DNA packaged in capsid proteins. They are around 2.0–31kb in length. It can be considered a type of viral vector.

Nucleic acid analysis suggests a very long association of the viruses with the wasps (estimated 73.7 million years ± 10 million).

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. ~. IV has a less clear origin: although earlier reports found a protein p44/p53 with structural similarities to ascovirus, the link was not confirmed in later studies. As a result, the current opinion is that IV originated from a yet unidentified novel viral family, In either case, both genera were formed through a single integration event in their respective wasp lineages.

In the host, several mechanisms of the insect immune system can be triggered when the wasp lays its eggs and when the parasitic wasp is developing. When a large body (wasp egg or small particle used experimentally) is introduced into an insect's body, the classic immune reaction is the encapsulation by hematocytes. An encapsulated body can also be melanised in order to asphyxiate it, thanks to another type of hemocyte, which uses the phenoloxidase pathway to produce melanin. Small particles can be phagocytosed, and macrophage cells can then be also melanised in a nodule. Finally, insects can also respond with production of antiviral peptides. PolyDNAvirus protect the hymenopteran 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 a protein CrV1 that denatures actin filaments in hematocytes, so those cells become less able to move and adhere to the larvae. PolyDNAvirus can also act on melanisation, MdBV interferes with the production of phenoloxidase. Finally, polyDNAvirus can also produce viral ankyrins, that interfere with production of antiviral peptides. In some Ichnoviruses, Vankyrin can also prevent apoptosis, the extreme reaction of a cell to block viral propagation. The Ichnoviruses produce some proteins called vinnexins which have been recognized as homologous to the innexins of insects. They are responsible for the encoding of the structural units of the gap junctions. These proteins may alter the intercellular communication which could explain the disruption of the encapsidation process.

Another strategy used by parasitoid Hymenoptera to protect their offspring is production of virus like particles. VLPs are similar to viruses in their structure, but they don't carry any nucleic acid. For example, Venturia canescens (Ichneumonidea) and Leptopilina sp. (Figitidaea) produce 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 calyx cells before they go to the oviducts. Work in 2006 did not find their link to any viruses and assumed a cellular origin. 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. Venturia canescens uses these instead of polydnaviruses because its ichnovirus has been deactivated. The Leptopilina VLPs or mixed strategy extracellular vesicles (MSEVs) contain some secretion systems. Their evolutionary picture is less clear, but a recently reported virus, L. boulardi Filamentous Virus (LbFV), shows significant similarities.

MicroRNA are small RNA fragments produced in the host cells thanks to a specific enzymatic mechanism. They promote viral RNA destruction. MicroRNA attach to 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) or RNAi (RNA interference.) It is interesting to consider the microRNA phenomenon in the polyDNAvirus context. Many hypotheses can be formulated:
Braconidae carry nudivirus related genes in their genome, so they may be able to produce microRNA against nudivirus, as an innate immunity. Wasps perhaps use microRNA to control the viral genes they carry. PolyDNAvirus can also use PTGS to interfere with the host's gene expression. PTGS is also used for organisms' development, using the same enzymes as antiviral gene silencing, so we can imagine that if the host uses PTGS against polyDNAvirus, perhaps it also affects its development.