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

TRSV or not TRSV, that is the question. In bees, obviously.

25 February, 2014

I promised some time ago now to blog on the exciting topic of whether or not a plant virus is infecting honeybees – and here it is!  I was also contacted by the legendary Dr Adrian Gibbs about this paper, because he has read this blog, so I am including a commentary from him as well.

A little while ago, Ji Lian Li and co-workers published a paper entitled “Systemic Spread and Propagation of a Plant-Pathogenic Virus in European Honeybees, Apis mellifera” in ASM’s Open Access journal mBio.  They stated that:

“Pathogen host shifts represent a major source of new infectious diseases. Here we provide evidence that a pollen-borne plant virus, tobacco ringspot virus (TRSV), also replicates in honeybees and that the virus systemically invades and replicates in different body parts. In addition, the virus was detected inside the body of parasitic Varroa mites, which consume bee hemolymph, suggesting that Varroa mites may play a role in facilitating the spread of the virus in bee colonies. This study represents the first evidence that honeybees exposed to virus-contaminated pollen could also be infected and raises awareness of potential risks of new viral disease emergence due to host shift events. About 5% of known plant viruses are pollen transmitted, and these are potential sources of future host-jumping viruses. The findings from this study showcase the need for increased surveillance for potential host-jumping events as an integrated part of insect pollinator management programs”.

This paper has caused all sorts of excitement, as well as coming to some possibly misleading conclusions, and leading to quite a lot of uninformed speculation – so I think it is as well to explore quite carefully what they did.

Adrian first:

“This paper reports that tobacco ringspot nepovirus, a well-known virus of plants, replicates in honeybees.  TRSV, first identified nearly a century ago in the USA, has a wide range of plant hosts, and is spread in pollen and seed, and also by many unrelated vectors, not only root-feeding nematodes, like other nepoviruses, but also insects and mites.

This report tells us that TRSV virions have been isolated from bees, and that their gene sequences are closely similar to those of TRSV.  Convincingly, biochemical tests showed that there were replication intermediates of the TRSV genome in the bees, so the virus had not merely contaminated the bees when they fed on the honey and pollen of infected plants, but had seemingly multiplied in them.

However, there are several gaps in this story.  Surprisingly, it seems that no tests were done to show whether the virus isolated from bees infected known plant hosts of TRSV; perhaps this crucial evidence will be in the sequel.  Furthermore, the reported sequences of the virus represented only around 20% of the RNA1 of typical nepoviruses, and around 50% of their RNA2, so there is still the possibility of further genetic surprises when the genome sequence is completed.

Although TRSV is a well-known and long studied virus with many distinct symptom variants, there are relatively few of its gene sequences in Genbank.  When these are compared with those of the ‘bee TRSV’ it is obvious that more sequences will be required to sort out exactly where this virus clusters; differences in the homology patterns of the RNAs 1 and 2 suggest that recombination or reassortment is active among nepoviruses.

The gene sequencing revolution is, to paraphrase Pliny the Elder, revealing that in virology the only certainty is that nothing is certain.”

Me next:

I have the same reservations as Adrian: the TRSV sequence isolated from bees and from Varroa mites is only partial (~30%); thus, it is by no means certain that the whole genome is colinear with genomes of established TRSVs or of other nepoviruses, although they assume that it is – with some justification, possibly, as sequence identities of up to 96% were found in Genbank for the putative CP fragment sequence.  They could isolate particles: why, then, in this metagenomic and NGS age, could they not sequence the whole thing??

nepo fig1

Another reservation I have concerns their methodology.  First, while I was impressed that they did strand-specific PCR to show  both the presence of viral (+ strand) and of replicative form (- strand) RNA in bee and mite tissue (see their Figure above), and did in situ hybridisation to show (-) strand presence in mites, they did not do something very simple that could have shown the same thing, AND given them genome-length +/- strand RNA to play with.

I refer, of course, to dsRNA isolation, which is a very easy and extremely clean technique that can be used to get full-length dsRNAs for many (+) strand RNA viruses from plant or insect tissues.  Moreover, the simple fact of isolating dsRNA forms for a single-strand RNA virus is indicative that replication is occurring – and was used by our group as long ago as 1988 (C Williamson, PhD Thesis, UCT) to isolate full-length ~10 kb dsRNA for two aphid picorna-like viruses.

Scan 04 Jan 2014, 16.31-page8

This means they could have had clear and simple evidence via dsRNA extraction of ALL of the coinfecting viruses present – without all of the expense of total cDNA sequencing.  And sampled more hives….

Second, I have to echo Adrian: “…no tests were done to show whether the virus isolated from bees infected known plant hosts of TRSV”.  Why ever not?  I am afraid that if I were a referee, I would have insisted on this: they did enough other work, after all, that this would not exactly have been an onerous requirement!

And here’s another thing: the authors say, in their Discussion,

“The finding from this study illustrates the complexity of relationships between plant pathogens and the pollinating insects and emphasizes the need for surveillance for potential host-jumping events as an integrated part of insect pollinator conservation.”

Ummmm…no, it doesn’t.  This is overstating the significance of their results by an order of magnitude at least.  They have simply illustrated that ONE species of honeybee may be infectable by ONE species of plant virus, and that this is ASSOCIATED with “weak” colonies.  Moreover, while the presence of TRSV was apparently associated with four weak colonies (out of only ten surveyed), it is quite possible that this is simply the emergence of a commensal-type infection against a background of known bee viruses, and in particular Israeli acute paralysis virus which was found in the same colonies (and blogged on here).  The authors also seem to take it as a given that the “emergence” of TRSV into bees is a recent jump – when it may not be recent at all.  Their statement in the abstract that

“The tree topology indicated that the TRSVs from arthropod hosts shared a common ancestor with those from plant hosts and subsequently evolved as a distinct lineage after transkingdom host alteration”

is pretty much unsubstantiated, in the absence of any investigation of the lineage in plants or in other bee colonies.  Further, they say that

“This study represents a unique example of viruses with host ranges spanning both the plant and animal kingdoms. “

Ummmmm….it doesn’t really do that, either: there are a LOT of arboviruses, with quite a few of them infecting insects and plants.  Here, for example, is an illustration from my teaching material of why it is that I think that viruses of insects and plants are an underappreciated evolutionary link for later evolution of viruses that got into mammals.

Transkingdom viruses

I note that bunyaviruses, rhabdoviruses, reoviruses and (not shown) picorna-like viruses appear linked by the fact that insects have possibly the most diverse representatives of these families, which may indicate that these originated in insects.  Which were the first complex animals to crawl out of the oceans, to join…plants on dry land?  Which explains how plants link up with the far more closely related (in evolutionary terms) insects and vertebrates: plants and insects were alone together for a long, long time before things with spines lurched up out of the water to join them.  So were their viruses.

I also said the following in the material there:

“A complicating factor in the picture of viruses co-evolving with their hosts over millennia is the fact that viruses apparently can – and obviously do – make big jumps in hosts every now and then.  It seems obvious, for example, that arthropods are almost certainly the original source for a number of virus families infecting insects and mammals - such as the Flaviviridae - and probably also of viruses infecting insects and other animals and plants - such as the Rhabdoviridae and Reoviridae - as well (see also here).  For example, picornaviruses of mammals are very similar structurally and genetically to a large number of small RNA viruses of insects and to at least two plant viruses, and – as the insect viruses are more diverse than the mammalian viruses - probably had their origin in some insect that adapted to feed on mammals (or plants) at some distant point in evolutionary time.”

Now quite a lot of interest has been shown in this paper in the blogosphere, and there have been quite a few conclusions drawn from the results that I think are largely unsubstantiated.  For example, this Sci Am blog claims

“When HIV jumped from chimpanzees to humans sometime in the early 1900s, it crossed a gulf spanning several million years of evolution. But tobacco ringspot virus, scientists announced last week, has made a jump that defies credulity. It has crossed a yawning chasm ~1.6 billion years wide.”

Again, ummmm…in light of the discussion above, not necessarily!  I am of the opinion that picorna-like viruses were shared between insects and plants, and then between insects and animals, hundreds of millions of years ago.  And TRSV is a nepovirus – and nepoviruses look like nothing more or less than a picornavirus with a divided genome.

I think TRSV represents something coming back into insects.  And I think we will probably find a lot more of them.

GM crops: European scientists descend on Africa to promote biotech

24 February, 2014

See on Scoop.itVirology News

Africa is expected to be the next target of GM food companies, as European scientists and policymakers travel to Ethiopia to boost the prospect of growing more of the controversial crops on the continent.

Anne Glover, the chief scientific adviser to the European commission, and other prominent pro-GM researchers and policymakers from European countries including Germany, Hungary, Italy and Sweden will this week meet Ethiopian, Kenyan, Ghanaian and Nigerian farm ministers as well as officials from the African Union.

Ed Rybicki‘s insight:

And that’ll go down REALLY well: European governments and policymakers pushing GM crops in Africa, when their own people don’t want them?  

Whether those reasons are stupid or not, and whether or not it is a good idea to plant GM in Africa, I can see a knee-jerk anti-Europe response could well work to completely screw up just what it is they are trying to do.

Consider: Zimbabwe and Zambia resolutely oppose even the import of GM maize as FOOD, let alone allowing the planting of it.  Africans have a history of being VERY suspicious of outsiders bearing gifts – because there is a history of dumping stuff in Africa, of everything from suspect pharmaceuticals to excess chickens.

I predict a lead balloon result for this conference and for the initiative.  Time for Europe to listen to the Kenyans, Burkinabe and South Africans about the merits of growing GM – and not the other way around!

See on www.theguardian.com

South Africa unable to produce foot-and-mouth disease virus vaccine

20 February, 2014

See on Scoop.itVirology News

Outbreak of foot and mouth disease four years ago largely due to collapse of state’s ability to manufacture vaccines

THE outbreak of foot and mouth disease four years ago, which cost South Africa R4bn a year in lost exports, was largely due to the collapse of the state’s ability to manufacture vaccines.

Agriculture, Forestry and Fisheries Minister Tina Joemat-Pettersson told a press briefing on Wednesday on the lifting the ban of red meat exports by the World Animal Health Organisation (WAHO). The removal of the boycott will not affect red meat producers significantly as South Africa usually imports the product to satisfy domestic demand. Only about 1% of red meat production, mainly venison, is exported. Other animal exports include hides and wool.

Ed Rybicki‘s insight:

This is actually horrifying, in the context of what is SUPPOSED to be Africa’s most developed economy – and especially its most developed agricultural economy.

Really: it is a fact not much appreciated outside of the agricultural sector, that we have to get our FMDV vaccines from BOTSWANA.

That’s right – the country with the largest economy in Africa gets its FMDV vaccines from the Botswana Veterinary Institute, a factory set up by the French in a country with a total population about a quarter of that of Greater Johannesburg.

So, let us get this straight: the country that owns the Onderstepoort Veterinary Institute, where the legendary Sir Arnold Theiler pioneered virus and other vaccines from the 1890s on, cannot make its own FMDV vaccines any more?

The country that USED to make a whole range of animal vaccines via the state-owned facility that is now Onderstepoort Biological Products, is now struggling to make just a few?

The country that once built a state-of-the-art BSL4 facility dedicated to FMDV now cannot operate it, or even make old-style killed vaccines?

Don’t let me get started on human vaccines, because we now don’t make ANY – but the erosion of our capacity to make vaccines means our ability to look after human and animal health is now severely under threat.

See on www.bdlive.co.za

Eat your vaccines

7 February, 2014

See on Scoop.itVirology and Bioinformatics from Virology.ca

Vaccines have been revolutionary in medicine, but why are they not used in some parts of the world and how can they be improved? …

Ouch! Wouldn’t it be great if instead of a jab with a needle, you could just eat a vaccine instead? Luckily, researchers at the University of California agree, and their attempts to use algae to produce an edible malaria vaccine is just one example of the many strides forward scientists are taking in vaccine research.

Ed Rybicki‘s insight:

I love these idealistic but naive statements about how plant-production-of-vaccines-will-let us-get-away-from-needles: very 1990s; a little out of touch with modern realities – unfortunately!

The facts are that any edible (read: oral) vaccine will have to be regulated as tightly as an injectable, in terms of dose and administration.

Really: giving too little OR too much; giving it too often or not often enough; giving a product that has not been QCed or checked for potency  after storage…is suicide, in the vaccine world.

Even if it IS safe enough to eat.

See on www.isciencemag.co.uk

RNA sequencing of 750-year-old barley virus sheds new light on the Crusades

7 February, 2014

See on Scoop.itVirology News

Scientists have for the first time sequenced an ancient RNA genome – of a barley virus once believed to be only 150 years old – pushing its origin back at least 2,000 years and revealing how intense farming at the time of the Crusades contributed to its spread.

Ed Rybicki‘s insight:

This is a good report about a VERY interesting finding – with one flaw.  They go on, apparently, about how BSMV is a "new virus": why would anyone think that?  Since the late 1980s, Adrian Gibbs and others have pointed out that tobamoviruses are probably ancient; just because RNA CAN evolve fast doesn’t mean it does, in terms of encoding functional elements.  Gibbs showed this for plant viruses; it has also been done for the HIV/SIV complex, where it is shown that a similar divergence in sequence among theses viruses to all animals since the Cretaceous, has led to NO changes in morphology, or gene function.

The simple fact is that having "plastic" genome in comparison to eukaryotic cells does NOT mean that ssRNA viruses may not be ancient.

Having said all that, it really is a tour de force to have sequenced a virus that old – aided by the fact, I am sure, that BSMV is hardy little beast, with a really stable vision.

Now, to find those hundred-year-old maize leaves put away with maize streak virus symptoms….B-)

Thanks to @Elsevier Microbiol* for pointing this out!

See on www.sciencedaily.com


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