I have taught – when I did teach that is, two years ago now – for years that most plant viruses are transmitted by one or other form of vector, and that this transmission is very often relatively specific, even though it usually does not involve multiplication of the virus in the vector. Unfortunately, this is an under-studied area (like most of plant virology), and even more so now in this era of folding plant virology into “biotic stress” and other concocted disciplinary areas.
However: amid the gloom is a bright light (or two – see here as well for some local SA news), and it comes from a PLoS Pathogens paper entitled “Structural Insights into Viral Determinants of Nematode Mediated Grapevine fanleaf virus Transmission” [need to leave out the italics there, guys; only a species name as an abstract concept gets italicised, and this is an entity you’re talking about!].
Schellenberger P, Sauter C, Lorber B, Bron P, Trapani S, et al. (2011). PLoS Pathog 7(5): e1002034. doi:10.1371/journal.ppat.1002034
Many animal and plant viruses rely on vectors for their transmission from host to host. Grapevine fanleaf virus (GFLV), a picorna-like virus from plants, is transmitted specifically by the ectoparasitic nematode Xiphinema index. The icosahedral capsid of GFLV, which consists of 60 identical coat protein subunits (CP), carries the determinants of this specificity. Here, we provide novel insight into GFLV transmission by nematodes through a comparative structural and functional analysis of two GFLV variants. We isolated a mutant GFLV strain (GFLV-TD) poorly transmissible by nematodes, and showed that the transmission defect is due to a glycine to aspartate mutation at position 297 (Gly297Asp) in the CP. We next determined the crystal structures of the wild-type GFLV strain F13 at 3.0 Å and of GFLV-TD at 2.7 Å resolution. The Gly297Asp mutation mapped to an exposed loop at the outer surface of the capsid and did not affect the conformation of the assembled capsid, nor of individual CP molecules. The loop is part of a positively charged pocket that includes a previously identified determinant of transmission. We propose that this pocket is a ligand-binding site with essential function in GFLV transmission by X. index. Our data suggest that perturbation of the electrostatic landscape of this pocket affects the interaction of the virion with specific receptors of the nematode’s feeding apparatus, and thereby severely diminishes its transmission efficiency. These data provide a first structural insight into the interactions between a plant virus and a nematode vector.
And yes, they do – and illuminate very nicely the concept of structural complementarity as a means of ensuring specific transmission by any vector of a plant virus. That this can happen in the absence of any replication of the virus in the vector, as is the case here and in fact for most plant virus / vector associations, indicates that an evolutionary process that probably started with fortuitous low-efficiency transmission by pure random chance of an ancestor GFLV by the nematode, resulted in selection of increasingly more efficiently transmitted viral variants.
The same sort of thing has undoubtedly happened for specific aphid transmission of viruses like Cucumber mosaic virus and other cucumoviruses [note to virologists: correct usage!] and Potato virus Y and other potyviruses, and my favourite geminiviruses.
I look forward to an explosion of research in this area, not the least because it may lead to simple agents that specifically block the transmission. One can hope…B-)