Working on the assumption that it’s always best to know where you might contract something that could kill you, Google brings you….dengue!
Archive for May, 2011
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-)
So it is, again, we are driven to report evidence-based absence of evidence for a very contentious virus: the murine retrovirus known as XMRV. From a preprint online publication in Journal of Virology:
Absence of XMRV and other MLV-related viruses in patients with Chronic Fatigue Syndrome
J. Virol., published ahead of print on 4 May 2011 doi: doi:10.1128/JVI.00693-11
Clifford H. Shin, Lucinda Bateman, Robert Schlaberg, Ashley M. Bunker, Christopher J. Leonard, Ronald W. Hughen, Alan R. Light, Kathleen C. Light, and Ila R. Singh
“Chronic fatigue syndrome (CFS) is a multi-system disorder characterized by prolonged and severe fatigue that is not relieved by rest. Attempts to treat CFS have been largely ineffective primarily because the etiology of the disorder is unknown. Recently CFS has been associated with xenotropic murine leukemia virus-related virus (XMRV) as well as other murine leukemia virus (MLV)-related viruses, though not all studies have found these associations. We collected blood samples from 100 CFS patients and 200 self-reported healthy volunteers from the same geographical area. We analyzed these in a blinded manner using molecular, serological and viral replication assays. We also analyzed samples from patients in the original study that reported XMRV in CFS. We did not find XMRV or related MLVs, either as viral sequences or infectious virus, nor did we find antibodies to these viruses in any of the patient samples, including those from the original study. We show that at least some of the discrepancy with previous studies is due to the presence of trace amounts of mouse DNA in the Taq polymerase enzymes used in these previous studies. Our findings do not support an association between CFS and MLV- related viruses including XMRV and off-label use of antiretrovirals for the treatment of CFS does not seem justified at present.”
I would have said “enough said, then!” Except that this will not be the end. Oh, no….
From The Scientist of today:
“Another study fails to find XMRV in chronic fatigue patients
The latest in a string of studies searching for a mouse virus in patients suffering from chronic fatigue syndrome has failed to turn up evidence of the pathogen, XMRV. The study, which was published online last week in the Journal of Virology, couldn’t detect XMRV in 100 people with chronic fatigue syndrome, including 14 of the patients who tested positive in the 2009 Science study that originally posited a link between the virus and the syndrome. University of Utah in Salt Lake City virologist Ila Singh, who led the new study, suggests (as have others) that the XMRV previously found in chronic fatigue patients was a result of contamination in the lab. But Judy Mikovits, senior author of that 2009 Science paper and virologist at the Whittemore Peterson Institute for Neuro-Immune Disease, is standing by her findings. “We have complete confidence in every bit of the results in the Science paper,” she told ScienceInsider.”
Well, she would say that, wouldn’t she? And who would blame her…but time to start looking somewhere else, folks!