A new virus from the Namib – and a guilty secret revealed

26 June, 2014

I have to confess to a guilty secret: there is a pleasure-inducing activity I have been indulging in for a week at a time these past three years.

And not alone….

This consists of going to the Gobabeb Research & Training Centre in the Namib Desert as part of an international “scientific expedition” aimed at investigating microbial soil biodiversity in the sandy and stony desert round Gobabeb.  These were started by Professor Don Cowan when he was at the University of the Western Cape, and have fortunately continued now that he has moved to a new Institute at the University of Pretoria.

Typical quartz-associated hypolith

Typical quartz-associated hypolith

I put the scientific expedition in quotes because anything that much fun shouldn’t be called scientific, but hey, it’s already resulted in one major paper on hypolith-associated viruses that I’m a minor author on, another co-authored opinion piece in the South African Journal of Science on biodiversity assessment that got the cover, as well as me being invited to be part of the Gobabeb station’s Microbiology & Fungi research “Theme Group“.

Moreover, I am now on the Board of the Institute for Microbial Biotechnology and Metagenomics at UWC on the strength of working with Marla Trindade and Lonnie van Zyl and others on scraping bits of green stuff off rocks and then watching them ultrafilter washings of it – so I suppose that we really did do some science, even if it was sinfully enjoyable. In any case, something that happened last year took me back to my roots – as well as possibly getting me some street (or gully) cred with the biodiversity crowd.

The heavily gullied area near Homeb

The heavily gullied area near Homeb

Basically, there we were in the Welwitschia-rich gullies near Homeb, 11 km from Gobabeb, visiting said plants.  There had been some rain 3 weeks previously, apparently, and there was an amazing eruption of foliage from some kind of bulb, every plant the same age and every one frantically flowering for all they were worth.  This alone was noteworthy, as the gullies were completely devoid of any trace of such plants the previous year. As we were wandering about, looking at Welwitschias, one Olivier Zablocki from the Univ Pretoria team – who had just done a MSc in plant virology with Gerhard Pietersen at UP – said something along the lines of “I wonder if there are any viruses infecting these plants?”.

welwitschia 2012

Welwitschia down in the gully

“What, like that one?” I said, having just fortuitously noticed a plant with tell-tale streaks on its leaves.  Of course, I seem to have lost my photos – temporarily, I hope! – after a Mac Mini OSX update disaster, but Olivier was kind enough to provide the necessary:

diseased albuca

Streaky Albuca. Note how quickly the fruit has formed, just a couple of days after flowering.

This sparked a flurry of activity, with people being called to observe the plant, and going out and looking for more.

Which were not found: not one other plant, of the hundreds we saw there and nearer Homeb, had any streaks at all.  What is more, they were growing all up and down some of the more inhospitable gravelly and rocky slopes I have ever seen, meaning they had to be seriously drought-tolerant, given the unlikelihood of them ever being exposed to much water.  This meant they must be ephemeral, or putting out foliage and flowers only after rain – and I have never seen anything flower as fast; three days later they were already fruiting.

albuca 2013

Albuca growing in the gully

We made the collective decision that this was sufficiently scientifically interesting to warrant its collection, and the plant was carefully dug up – with difficulty; the onion-like bulb was deep and seriously embedded among rocks – and carefully transported back to Gobabeb, hopefully for identification and then packaging to be taken back to Pretoria.

healthy albuca

Healthy Albuca growing in gravel

And yes, we did have a permit!

Meaning the foliage could go back to Pretoria, and there be subjected by Olivier to electron microscopy, and then RNA isolation and cDNA synthesis.  And lo, it came to pass – that a new potyvirus was discovered.  Kudos, Olivier and the Cowan lab!  The ms is submitted, and we wait only for…well, acceptance would be nice, but the proof is in the sequence.  And the pictures – murky EMs done by Olivier from precious tissue extracts, to boot.

Transmission EM from diseased Albuca extract

Transmission EM from diseased Albuca extract

And it took an old plant virologist to find it.  Life in the greying dog yet!

HPV type 16 E7 protein bodies cause tumour regression in mice

26 May, 2014

See on Scoop.itIIDMM News

Background

Human papillomaviruses (HPV) are the causative agents of cervical cancer in women, which results in over 250 000 deaths per year. Presently there are two prophylactic vaccines on the market, protecting against the two most common high-risk HPV types 16 and 18. These vaccines remain very expensive and are not generally affordable in developing countries where they are needed most. Additionally, there remains a need to treat women that are already infected with HPV, and who have high-grade lesions or cervical cancer.

Methods

In this paper, we characterize the immunogenicity of a therapeutic vaccine that targets the E7 protein of the most prevalent high-risk HPV – type 16 – the gene which has previously been shown to be effective in DNA vaccine trials in mice. The synthetic shuffled HPV-16 E7 (16E7SH) has lost its transforming properties but retains all naturally-occurring CTL epitopes. This was genetically fused to Zera(R), a self-assembly domain of the maize gamma-zein able to induce the accumulation of recombinant proteins into protein bodies (PBs), within the endoplasmic reticulum in a number of expression systems.

Results

High-level expression of the HPV 16E7SH protein fused to Zera(R) in plants was achieved, and the protein bodies could be easily and cost-effectively purified. Immune responses comparable to the 16E7SH DNA vaccine were demonstrated in the murine model, with the protein vaccine successfully inducing a specific humoral as well as cell mediated immune response, and mediating tumour regression.

Conclusions

The fusion of 16E7SH to the Zera(R) peptide was found to enhance the immune responses, presumably by means of a more efficient antigen presentation via the protein bodies. Interestingly, simply mixing the free PBs and 16E7SH also enhanced immune responses, indicating an adjuvant activity for the Zera(R) PBs.

 

I thank Russell Kightley Media for use of the HPV/cervical cancer graphic

Ed Rybicki‘s insight:

I keep saying – you gotta go green…B-) And here we are, suiting action to words.  

Modestly, of course.  

Well done to Mark Whitehead and Thomas Oelschlager; thanks to Inga for sticking with a difficult ms – and thanks Era Biotech for the technology!

See on www.biomedcentral.com

Virus experiments risk unleashing global pandemic, study warns

21 May, 2014

See on Scoop.itVirology News

Benefits of scientific testing in the area are outweighed by risks of pathogenic strains spreading round world, say researchers

Ed Rybicki‘s insight:

…and others say "Rubbish!"  I particularly like this bit:

 

"[Ron] Fouchier said…the authors had misinterpreted published data to arrive at their risk of someone picking up a virus in the laboratory. "The truth is that scientific research has never triggered a virus pandemic.""

The report goes on to say:

"Lipsitch and Galvani point out that a flu strain that spread around the world from 1977 to 2009 was probably released in a laboratory accident."

Yes.  But.  That was from the old Soviet Union – and they had a number of nasty things escape from laboratories, including anthrax and weaponised smallpox, by all accounts.

 

See on www.theguardian.com

An ACTUAL killer virus that could rise from the grave

1 May, 2014
Section through Variola virus.  Copyright Russell Kightley Media

Section through Variola virus. Copyright Russell Kightley Media

Having poo-pooed the possibility of killer viruses roaring out of the tundra to kill as all – see here – I find myself having to reconsider my words.  Just slightly, mind, but a reconsideration nonetheless.

This is because of an excellent post in Nature News recently, entitled “Infectious diseases: Smallpox watch“, by Sara Reardon.  This has raised quite a stir in the Twittersphere, as people speculate on just how likely this is, but I think the article itself does a very good job of discussing the possibility that smallpox could come back from the grave(s).

I have discussed smallpox a number of times in this blog, with one of the most read posts being this one by my PhD student (and now postdoc) Alta van Zyl.  I recall a while back a discussion around just how likely it was that people working on expanding what was the Rietfontein Infectious Diseases Hospital (now Sizwe Hospital)’s premises in Johannesburg, would find live smallpox in coffins of people who died of it at the old Hospital and were buried nearby.

The verdict then was “No” – Johannesburg is too hot, and the was seen to be NO chance of the virus surviving the rapid putrefaction that occurs in these parts.

Sara Reardon’s essay, however, raises the real, if rather remote, prospect of there being live smallpox in mummified corpses which have either dried out at low temperatures, or been frozen soon after death, in permafrost.  She says that

“A more likely source of infectious virus would be frozen bodies. Influenza viruses seem to be able to survive freezing in lakes and may thereby infect migrating birds…”

Now the good thing is that people have actually gone out looking for live virus in just such potential sources, and found nothing except fragments of DNA.

However, she also says:

“Another concern is that smallpox could escape from a secret cache. Few biosecurity specialists believe that the two stocks kept at the CDC and VECTOR are the only ones in existence. For instance, variola could very well be in the freezer of someone who defected from the Soviet Union…”

Now, the old Soviet Union had an active programme on weaponising smallpox, with some sources claiming than “several tonnes” of material were eventually made.  There is even evidence that smallpox escaped from a facility in Aralsk, Kazakhstan, in 1971.   What is not so clear is where any of this material is NOW, and in what state it is.

Time to work on the emergency-response smallpox vaccines and strategies, folks – even if you use the potential threat of monkeypox as the reason!

 

 

Recombinant Bluetongue virus vaccines – or some, anyway

1 May, 2014
VIRUS-rota-200

General model of reo-like viruses. Copyright Russell Kightley Media

I picked up yesterday – via @MicrobeTweets’ Twitter feed – on a very useful list of papers in a “Virtual Special Issue” of Elsevier’s recent coverage of vaccines – for “World Immunization Week”. Great stuff, I thought to myself, as I browsed the list – and downloaded at least those that were Open Access, or which I can get via our Libraries’ IP range.

“Even better!”, I thought, as I saw a review entitled “Recombinant vaccines against bluetongue virus?”  A meaty, well-sourced review, I thought; good reading for me and my students / coworkers, and good meat for upcoming Introductions for papers yet to be written.  Indeed, it promised the following:

“The multiple outbreaks of BTV in Mediterranean Europe in the last two decades and the incursion of BTV-8 in Northern Europe in 2008 has re-stimulated the interest to develop improved vaccination strategies against BTV. In particular, safer, cross-reactive, more efficacious vaccines with differential diagnostic capability have been pursued by multiple BTV research groups and vaccine manufacturers. A wide variety of recombinant BTV vaccine prototypes have been investigated, ranging from baculovirus-expressed sub-unit vaccines to the use of live viral vectors. This article gives a brief overview of all these modern approaches to develop vaccines against BTV including some recent unpublished data.”

So, I parked the conveniently Open Access-ible window away on the side of my desktop, to be got back to with every expectation of delight.

Until I read it, that is: well-sourced it may be; excellent in its coverage, it is NOT.  In fact, apart from a brief discursion on subunit vaccines – concentrating almost exclusively on baculovirus / insect cell-produced proteins – it is almost exclusively concerned with live viral vectors for bluetongue proteins, and of poxviruses in particular.  Now, this is all very well, if that is what they work on – but to dismiss one of the potentially most exciting developments in recent Bluetongue vaccinology like this:

“VLPs of BTV have been also produced in plants recently using the cowpea mosaic virus and their use in a vaccination study produced no clinical manifestations in sheep after homologous challenge, although viremia was no [sic] evaluated (Thuenemann et al., 2013).”

- boggles the mind somewhat.  Really?  That’s all they have, compared to the screed immediately before it on baculovirus-produced antigens?  They get the expression system wrong – it is an Agrobacterium tumefaciens-mediated transient expression system in Nicotiana benthamiana involving a Cowpea mosaic virus-derived enhanced translation vector – and neglect to mention that the VLPs produced are as good as anything produced in insect cells; will be FAR cheaper to produce, and WORKED AS WELL AS THE CONVENTIONAL ATTENUATED LIVE VIRUS VACCINE IN A CHALLENGE EXPERIMENT IN SHEEP.  True!

This is a big deal, folks, really: successful production of significant amounts of VLPs requiring simultaneous expression of 4 structural proteins of BTV-8 in plants AND their subsequent assembly, AND performing as well as the standard vaccine in an animal trial.  But no – not good enough for our review’s authors….

I must declare vested interests up front here: first, we work on plant-made recombinant Bluetongue vaccines; second, I and others in my group are co-authors of the paper whose lack of coverage I am aggrieved about.

But that’s not the point: what IS the point is that this review is a slipshod piece of work that damns our collective endeavour with faint praise, in community that might otherwise have been alerted to an alternative to the far-too-expensive-for-animal-use baculovirus expression technology.

Ah, well.  I suppose that’s what blogs are for B-)

Giant Zombie Killer Virus Rises From Its 30 000 Year Grave To Kill Us All! Or Not?

27 March, 2014

I am not a fan of “Science By Hype”, which I think I have made abundantly clear via Virology News and elsewhere. Thus, I pour scorn on the “We found a structure which will lead to an AIDS vaccine”, and “We found an antibody that will cure AIDS” type of articles, WHILE at the same time, appreciating the ACTUAL science behind the hype.

If there is any, of course.

Which is why I am torn, on the subject of a giant DNA virus purportedly found in 30 000 year-old Siberian permafrost. I am also a fan of zombies, hence the title. But seriously, now: here we are, with news media and semi- and fully-serious science mags all hailing the description in PNAS, no less, of “Pithovirus sibericum“.  A giant virus, wakened from a 30 000 year sleep in Siberian permafrost, by the kiss of an amoeba. OK, by infecting an amoeba, but you see where I’m going here. Pithovirus_sibericum__Researchers_Resurrect_30_000-Year-Old_Giant_Virus___Biology___Sci-News_com So here we are, with an article from Sci.news.com, trumpeting the discovery.  And there’s more:

“The findings have important implications in terms of public health risks related to the exploitation of mining and energy resources in circumpolar regions, which may arise as a result of global warming. “The re-emergence of viruses considered to be eradicated, such as smallpox, whose replication process is similar to Pithovirus, is no longer the domain of science fiction. The probability of this type of scenario needs to be estimated realistically.””

Yeah.  Rii-ii-ght.  Giant viruses are going to erupt from the permafrost and kill us all!  Really??

No.

Curtis Suttle, he of oceanic metaviromes fame, is quoted as saying the following, in Ed Yong’s Nature blog:

“…people already inhale thousands of viruses every day, and swallow billions whenever they swim in the sea. The idea that melting ice would release harmful viruses, and that those viruses would circulate extensively enough to affect human health, “stretches scientific rationality to the breaking point”, he says. “I would be much more concerned about the hundreds of millions of people who will be displaced by rising sea levels.””

Amen!  In other words, just because there ARE revivable viruses in permafrost – itself no new thing, BTW – does NOT mean they will harm humans. Think about this a moment: something locked away under the surface of the ground for 30 000+ years has to SURVIVE, first; second, it has to INFECT humans if it is to cause any harm. And what evidence do we have that anything found in Siberian permafrost can do that?

None.  None whatsoever.

Think again: how many humans, and how many mammals with virus that could infect humans, were there around on the Siberian plains 30 000 years ago?

Precious few.

And what likelihood is there that any viruses that COULD infect humans, got preserved? Vanishingly small. So what COULD get released from said permafrost, as it melts with inexorable global warming? Well, phages: lots and lots of phages.

Then some plant viruses, maybe: there have been previous reports of Tomato mosaic virus found in 1999 in glacial ice from Greenland, that was between 500 – 140 000 years old – that was also supposed to be a threat, as it escaped from melting icecaps.

To tomatoes, possibly.  If they grew in seawater.

But there’s more: here we have “New Deadly Flu Viruses Reemerge from Melting Ice“, from 2006.  Here we have

“An international team [that] found flu viruses in the ice of Siberian lakes, fact that warns about the possibility that global warming may release germs locked in glaciers for decades or even centuries.”

Yah. Right.  But at the same time, considerably more worthy of alarm than Pandoraviruses. Because what our worthy French colleagues did NOT do, in their report in PNAS, was see what ELSE was in their permafrost samples. Seriously: they trawled melting ice from a core sample with amoebae ONLY.

This is the equivalent of the 2nd year prac I used to do, when we made students screen water obtained from the environment with E coli to see if they could amplify coliphages out of it.  Why did they not do a metagenomic sequence trawl, after filtering out bits of mammoth crap and cockroaches and bits of twigs??  What did they MISS?  HBVs that infected Denisovans?  And are we SURE that the virus came from that long ago?  Has the ice really remained frozen all that time – and is there not the possibility that water didn’t percolate down through cracks and pores in the permafrost, carrying the virus with it, from a more clement environment on the surface??

OK, OK, so it’s a great find, and reasonably worthy of SOME hype.  BUT: it is NOT a harbinger of doom, because most viruses will NOT survive 30 000 years worth of entombment in ice, and in any case, would NOT infect humans even if they did. AND I hate the name: “Pithovirus sibericum“?  Really??  Viruses are not named like that!  Except by French folk who find these strange “amphora-shaped” viruses, apparently.

The Assembly Pathway of an Icosahedral Single-Stranded RNA Virus Depends on the Strength of Inter-Subunit Attractions

27 March, 2014

See on Scoop.itVirology News

The strength of attraction between capsid proteins (CPs) of cowpea chlorotic mottle virus (CCMV) is controlled by the solution pH. Additionally, the strength of attraction between CP and the single-stranded RNA viral genome is controlled by ionic strength. By exploiting these properties, we are able to control and monitor the in vitro co-assembly of CCMV CP and single-stranded RNA as a function of the strength of CP–CP and CP–RNA attractions. Using the techniques of velocity sedimentation and electron microscopy, we find that the successful assembly of nuclease-resistant virus-like particles (VLPs) depends delicately on the strength of CP–CP attraction relative to CP–RNA attraction. If the attractions are too weak, the capsid cannot form; if they are too strong, the assembly suffers from kinetic traps. Separating the process into two steps—by first turning on CP–RNA attraction and then turning on CP–CP attraction—allows for the assembly of well-formed VLPs under a wide range of attraction strengths. These observations establish a protocol for the efficient in vitro assembly of CCMV VLPs and suggest potential strategies that the virus may employ in vivo.

 

Ed Rybicki‘s insight:

I do love it when a paper is published that could have been done pretty much any time in the last 40 years – and with one of my favourite viruses, that I played with a LOT back there before 1980.

Ultracentrifugation, pH meters, ionic strength determinations, EM…all tried and true, and used 40+ years ago. OK, they also used cloned BMV RNA 1 cDNA, and did 3-D image reconstruction from EMs, but hey, they needn’t have done that!  Nice, straightforward physicochemical studies, on a well-characterised virus, with good, simple conclusions. 

Namely, that assembly of the virus is NOT just a simple mix-CP-and-RNA-and-it-will-happen, but that it depends upon both pH, for modulating ionic interactions,and ionic strength for modulating ionic interactions AND the "hydrophobic effect", as we used to know it.

While their conclusions are relevant for assembly of heat- and nuclease-resistant nano particles in vitro, I wonder if they are physiologically relevant: if "correct" assembly depends upon first, turning on CP-RNA attraction (ionic strength shift), and second, turning on CP-CP attraction (pH shift) – where in the cell does that happen?

In their own words, "It is generally accepted that the cytoplasm of plant cells is maintained near neutral pH with ionic strength of approximately 0.1 M. Our in vitro results show that these conditions are insufficient for nucleocapsid formation in the absence of cellular host factors."

Yeeee-ee-eesssss…precisely. What happens in the cell? The answer could lie in the one thing they don’t report, but that some of the heroes of my distant youth – people like JB Bancroft and Thom Hohn, both quoted (from 1970 and 1969 respectively) in this paper, DID do. Namely, investigate what happens at different CP and RNA concentrations, at constant pH and ionic strength.

You see, it was shown 30+ years ago – and I have been lecturing on it since then – that CP and RNA for viruses like BMV / CCMV and MS2 form different complexes with their cognate partners at different molecular ratios. That is, at low CP:RNA ratios, a high-affinity complex is formed, which is basically a ribonucleoprotein complex without structure. Increasing the CP:RNA ratio for both MS2 and CCMV, as I recall (maybe Dick Verduin was involved with CCMV), results in further lower-affinity association of CP with both RNA and already-bound CP – which acts as a nucleation complex – to result in full capsid assembly.

I note that the process in both cases was shown to be specific, for low CP:RNA ratios: that is, it was cognate CP and RNA doing the high affinity nucleation complex formation.

And these guys deliberately used a heterologous RNA…albeit one from a related virus, but still: what would have happened if they’d used CCMV RNA?

Still – great paper, taking me back to when I wrote an essay on "Assembly of Spherical Plant Viruses" in my Honours year in 1977, quoting quite a few of the same references these folk did. Ah, simpler times…B-)

See on www.sciencedirect.com

Antivaxer HPV nonsense!

14 March, 2014

Fair Lady magazine just published a short but very useful article on HPV vaccines, with question-and-answer format commentary from a number of local experts on safety and such.

Then some loony takes them on in this piece.

My comment to that:

OK: this is a sadly under-informed and over-complicated response to a very good, simple article, with expert comments that are no way out of line with what is known to be the case about these vaccines.

Please allow me to correct a few things: in the first place, you say “Several ingredients in the two HPV vaccines are known to be a problem. One is the use of the microbe Saccharomyces cerevisiae, common yeast, as the medium in which the Gardasil antigen is developed. S. cerevisiae is known to trigger autoimmune response, as discussed recently in Yeast in Vaccines Tied to Autoimmune Diseases. Cervarix, though, was produced with a different medium, Trichoplusiani.”

Yeast is known to trigger autoimmune responses? Really? Then what about all those millions of people who have received Hepatitis B virus vaccine, also made in yeast? There is NO documented correlation with vaccination with yeast-made products and autoimmunity. NONE.

Then, Cervarix is “made in a different medium” – you obviously mean cell type, because Trichoplusia ni [note!] is a species of insect, from which the tissue-cultured cells used to make the HPV vaccine are derived. And? You have no problem with that? You shouldn’t.

Further: “The two vaccines, Gardasil and Cervarix, are distinctly different in another way. Gardasil contains a single adjuvant… while Cervarix utilizes a combination …These differences, since they involve the hyper-activation of the immune system and a known trigger for autoimmune disorders in only one of the vaccines, suggest that a recent study’s finding that there are no adverse effects whatsoever in either vaccine beggar belief.”

So you have a problem with the finding that there are no adverse effects BECAUSE the adjuvant regime is different? Not because of the evidence? Sorry, that isn’t very good science!

And it gets better: “Most significantly, in every clinical trial evaluating safety for both Gardasil and Cervarix, the so-called placebo groups were given injections that included an active aluminum adjuvant!
Though this is a common practice in vaccine trials, it is obviously a blatant means of biasing the results.”

So – a perfectly acceptable placebo arm in a clinical trial, with adjuvant given so that any difference would not be due to just this, means the studies are meaningless? Really?? What about the UNvaccinated groups these were compared to? ALL vaccines are associated with SOME events – and I note that YOUR piece above contains the sentence “The high proportion of adverse events reported is mainly due to the design of the study, since women were requested to report all events occurring after the vaccination; however the majority of events were mild and transient”.

You then quote – at excruciating length – a number of articles purportedly supporting your case, that can be summarised as showing that “HPV vaccination does not have a therapeutic effect in young women with pre-existing human papillomavirus infection”.

Yes? And? The two licenced HPV vaccines are PROPHYLACTIC, and were never intended to be therapeutic! It is unfortunate that the vaccines do not in fact lessen ESTABLISHED infections; however, there is plentiful evidence that they PREVENT INFECTIONS FROM BEING ESTABLISHED.

You are being alarmist and spreading falsehoods from a very shaky evidential base. You should stop doing that, or risk being shown up as being an antivax crank.

This Old PI….

7 March, 2014

See on Scoop.itVirology News

Ed Rybicki‘s insight:

I blame Chris Upton

VIGS in fungi – using TMV?!

5 March, 2014

See on Scoop.itVirology News

RNA interference (RNAi) is a powerful approach for elucidating gene functions in a variety of organisms, including phytopathogenic fungi. In such fungi, RNAi has been induced by expressing hairpin RNAs delivered through plasmids, sequences integrated in fungal or plant genomes, or by RNAi generated in planta by a plant virus infection. All these approaches have some drawbacks ranging from instability of hairpin constructs in fungal cells to difficulties in preparing and handling transgenic plants to silence homologous sequences in fungi grown on these plants.

Here we show that RNAi can be expressed in the phytopathogenic fungus Colletotrichum acutatum (strain C71) by virus-induced gene silencing (VIGS) without a plant intermediate, but by using the direct infection of a recombinant virus vector based on the plant virus, tobacco mosaic virus (TMV). We provide evidence that a wild-type isolate of TMV is able to enter C71 cells grown in liquid medium, replicate, and persist therein. With a similar approach, a recombinant TMV vector carrying a gene for the ectopic expression of the green fluorescent protein (GFP) induced the stable silencing of the GFP in the C. acutatumtransformant line 10 expressing GFP derived from C71.

The TMV-based vector also enabled C. acutatum to transiently express exogenous GFP up to six subcultures and for at least 2 mo after infection, without the need to develop transformation technology. With these characteristics, we anticipate this approach will find wider application as a tool in functional genomics of filamentous fungi.

TMV graphic from Russell Kightley Media

Ed Rybicki‘s insight:

This is a nice paper for two main reasons: one, they were able to get VIGS – virus-induced gene silencing – working in a non-model fungus; two, they did it with TMV.

TMV! A plant virus in good standing, not previously shown to infect fungi productively, even if it has been studied in yeast as far as replication requirements go.

This is very interesting, not the least because it opens up the possibility that TMV NATURALLY infects some soil / leaf surface fungi.

Which could open up some investigation of just how the virus gets around, because it has always been touted as being only “mechanically” transmissible – even though we and others have shown it CAN be transmitted by aphids (reasonably inefficiently).

Mind you, Barbara von Wechmar and others in our lab showed in the 1980s that wheat stem and leaf rust fungi could transmit Brome mosaic virus and that Puccinia sorghi could transmit a potyvirus; they just did not have the techniques to look at whether or not it replicated too.

As far as my last post here is concerned, I think there is going to be a LOT of stuff coming out in the next few years on how “plant” and “insect” and “fungal” viruses are in fact considerably more promiscuous in choice of host(s) than we have hitherto been aware.

Now, just to prove what Barbara always said, that Tobacco necrosis virus is also a bacteriophage….

Thanks to Gary Foster (@Prof_GD_Foster) for pointing this out!

See on m.pnas.org


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