Archive for February, 2013

Vaccines: a simple message

28 February, 2013

+MaryMangan over there on Google+ made an interesting point about simple messages to refute the kinds of nonsense promulgated by vaccine denialists, among others.

Here’s my contribution:

Vaccines!

Vaccines!

Phages hijack a host’s defence

28 February, 2013

See on Scoop.itVirology News

“Bacteria have developed a formidable arsenal of sophisticated strategies to neutralize viruses, but phages always seem to find a way to evolve, persist and abound. Studies of the complex evolutionary dynamics between phages and bacteria led to the discovery of a widespread bacterial defence system called CRISPR/Cas. On page 489 of this issue, Seed et al. report the remarkable finding that some phages that infect the bacterial pathogen Vibrio cholerae have also acquired a functional CRISPR/Cas system in their own genome which allows them to neutralize an unrelated antivirus system in their bacterial host”

Ed Rybicki‘s insight:

So many people have pointed this out to me today that I just HAD to do something on it.

 

This is a seriously big deal, in our understanding of the arms race between viruses and their hosts: here we have a virus that is circumventing a widespread antiviral defence system in bacteria, by using elements of the system against the bacteria – and it can adapt to match its hijacked system to that of the host.

 

Not only stranger than we imagine; sometimes stranger than we CAN imagine – or just way more sophisticated than we thought.

See on www.nature.com

Boy’s death from bat virus sparks calls for action to reduce flying fox populations

25 February, 2013

See on Scoop.itVirology News

THE mother of a Cairns boy who died from lyssavirus on Friday has said no one should have to suffer the bat-borne virus’ deadly effects.

Ed Rybicki‘s insight:

And so the inevitable happens, and a sick little boy dies – from Australian bat lyssavirus infection.

Now, while I keep going on about "flying rats", one needs to get the "bat threat" in perspective: ONE child died in recent history due to a bat-borne rabies-like virus, and FOUR people since 1994 of bat-borne Hendra virus.  Yet people are calling for a cull: that’s right up there with the "kill all Great White Sharks" campaigns there have been over the years, for a threat of death of injury that is considerably less than you expereince every morning driving to work.

See on www.couriermail.com.au

US bird flu research to resume under new restrictions

25 February, 2013

See on Scoop.itVirology News

Back in January 2012, the US government announced it was joining with scientists around the world and temporarily suspending research on the deadly pathogen H5N1, also known as avian flu or “bird…

Ed Rybicki‘s insight:

" "the policy aims to preserve the benefits of life sciences research while minimizing the risk of misuse.""

 

OK – can’t argue too hard with that, I suppose?  EXCEPT that it probably limits access to the research of countries where the virus is ACTUALLY a problem.

See on www.theverge.com

Pulse polio vaccine administered

25 February, 2013

See on Scoop.itVirology News

As a part of pulse polio immunisation programme, over 5.63 lakh children below five years including new born babies were administered with oral polio vaccine in  the twin cities and cantonment area here on Sunday….

Ed Rybicki‘s insight:

Just shows you the sheer scale of the effort – nearly a million babies in ONE district in India! – still needed to contain a virus that was almost eradicated.  Almost, that is, until politics and selfish policies made people in neighbouring Pakistan suspicious of vaccinators.

See on newindianexpress.com

A geographic analysis of population density thresholds in the influenza pandemic of 1918-19

25 February, 2013

See on Scoop.itVirology News

Geographic variables play an important role in the study of epidemics. The role of one such variable, population density, in the spread of influenza is controversial.

Prior studies have tested for such a role using arbitrary thresholds for population density above or below which places are hypothesized to have higher or lower mortality. The results of such studies are mixed.

The objective of this study is to estimate, rather than assume, a threshold level of population density that separates low-density regions from high-density regions on the basis of population loss during an influenza pandemic. We study the case of the influenza pandemic of 1918–19 in India, where over 15 million people died in the short span of less than one year.

Pandemic recombinant influenza virus graphic from Russeel Kightley Media

Ed Rybicki‘s insight:

This is an interesting paper, because it is one of the ONLY ones I have ever seen that analyses ANYTHING to do with the 1918 H1N1 pandemic, that comes from a developing country.  Moreover, it makes what I think is possibly quite a valuable contribution to "health geographics", especially for high-denisty low-income populations.

I also note that 15 MILLION PEOPLE were estimated to have died in India ALONE: this is close to the old estimate for the WORLD total (20 million), which was revised upwards to 50-100 million after developing country stats were taken into account, in the late 1990s.

Makes you think what a new version might do….

 

 

See on 7thspace.com

TMV in mouse lungs: more thoughts and refutations

13 February, 2013

tmv sedimhave been thinking about this paper (see last post), and it and other people’s posts (eg: Tommy Leung’s) have prompted more response.

I note the authors  say the following:

“There is other published literature that challenges the dogma of the strict boundaries between plants and vertebrates for viruses. In non-vertebrate animals, it was shown that plant pathogenic viruses displayed complex interactions with insects, and the transcription and replication of some plant viruses within insects was described [29][32]. In addition, in some cases, insects were found to be affected by plant viruses [33]. Furthermore, it was recently shown that Tomato spotted wilt virus (TSWV) could infect two human cell lines, HeLa and diploid fibroblasts, depending on the expression of a viral polymerase-bound host factor[34]. Additionally, despite plant virus replication was not observed in animals, Cowpea mosaic virus (CPMV), a plant comovirus in the picornavirus superfamily, was able to bind and enter mammalian cells, including endothelial cells, and the binding protein for the virus was identified as a cell-surface form of the intermediate filament vimentin [35]. Furthermore, CPMV was found to persist for several days post oral or intravenous inoculation in a wide panel of body tissues in mice, including in the lung and the liver [36]. Additionally, it was demonstrated that TSWV induced a strong immune response in its insect vector Frankliniella occidentalis [37] and that oral administration of Cowpea severe mosaic virus, Alfalfa mosaic virus and chimeric plant virus particles induced a durable and systemic immune response in mice [38][39]

Yes.  Um. Well.  The “dogma of the strict boundaries between plants and vertebrates for viruses”?  I have been teaching virology for 32 years, and I am not aware of actual DOGMA – as in, “that which has to be believed”.  Rather, there has been the cumulative set of OBSERVATIONS that nothing that anyone has ever isolated out of a plant – and that replicates in it – has infected a vertebrate.  I make that distinction, because there is always the possibility that, as we and others have found with insect viruses, plants can act as a “circulative, non-propagative vector” for insect viruses (for Rhopalosiphum padi aphid virus in barley, from my lab, and Leafhopper A virus in maize) – and if one realises that male mosquitoes, and often also females, feed on plants…you see where I’m going here?  As in, it might well be possible for a virus that multiplies in an insect and also in a vertebrate, to POTENTIALLY be found in a  plant?

In ay case, this is largely beside the point, because the authors get sidetracked into discussing Tomato spotted wilt – which happens to be a plant-adapted bunyavirus, most closely related to insect and vertebrate phleboviruses – “depending on the expression of a viral polymerase-bound host factor”.  Really??  And if it isn’t there?  Does the virus in fact spread?  For that matter, my lab has cell-free translated two aphid picorna-like virus genomes in rabbit reticulocyte lysates, but we made no claim that it could happen in rabbit cells.  Moreover, they make much of the fact that “a plant comovirus in the picornavirus superfamily, was able to bind and enter mammalian cells…[and] was found to persist for several days post oral or intravenous inoculation in a wide panel of body tissues in mice, including in the lung and the liver”.

Yes?  And?  A REALLY stable plant virus was able to bind and enter animal cells, and persist?  The problem with that is…?

We in the virus-like particle vaccine field RELY on the fact that VLPs will be taken up by cells of the immune system in vertebrates, and that they will elicit immune responses – so why is this regarded as a problem?  In fact, TMV has itself been tested as an RNA vaccine delivery system, due to its ability to protect a RNA payload, and get itself delivered into reticulocytes and macrophages – meaning this property has been known for some time, and has not hitherto been seen as a problem!

I think these authors have hyped something that is quite interesting into what THEY regard as a potential problem, for the purposes of getting their article accepted – and I think this needs to be recognised, and that the perceived risks need to be minimised by the knowledgeable.

PLOS ONE: Tobacco Mosaic Virus in the Lungs of Mice following Intra-Tracheal Inoculation

13 February, 2013

See on Scoop.itVirology News

“Plant viruses are generally considered incapable of infecting vertebrates. Accordingly, they are not considered harmful for humans. However, a few studies questioned the certainty of this paradigm. Tobacco mosaic virus (TMV) RNA has been detected in human samples and TMV RNA translation has been described in animal cells. We sought to determine if TMV is detectable, persists, and remains viable in the lung tissues of mice following intratracheal inoculation, and we attempted to inoculate mouse macrophages with TMV. In the animal model, mice were intratracheally inoculated with 1011 viral particles and were sacrificed at different time points. The virus was detected in the mouse lungs using immunohistochemistry, electron microscopy, real-time RT-PCR and sequencing, and its viability was studied with an infectivity assay on plants. In the cellular model, the culture medium of murine bone marrow derived macrophages (BMDM) was inoculated with different concentrations of TMV, and the virus was detected with real-time RT-PCR and immunofluorescence. In addition, anti-TMV antibodies were detected in mouse sera with ELISA. We showed that infectious TMV could enter and persist in mouse lungs via the intratracheal route. Over 14 days, the TMV RNA level decreased by 5 log10 copies/ml in the mouse lungs and by 3.5 log10 in macrophages recovered from bronchoalveolar lavage. TMV was localized to lung tissue, and its infectivity was observed on plants until 3 days after inoculation. In addition, anti-TMV antibody seroconversions were observed in the sera from mice 7 days after inoculation. In the cellular model, we observed that TMV persisted over 15 days after inoculation and it was visualized in the cytoplasm of the BMDM. This work shows that a plant virus, Tobacco mosaic virus, could persist and enter in cells in mammals, which raises questions about the potential interactions between TMV and human hosts.”

Ed Rybicki‘s insight:

Interesting paper!  Which proves…which proves…which proves TMV is seriously resistant to degradation in animals and in mammalian cells; that it can enter macrophages; and that it…what?  What, exactly, are the “…questions about the possible interactions…”?  What would TMV do in mammalian cells?  Yes, it might be uncoated and be translated; it is far less likely that it MIGHT be able to replicate its RNA – and then?  While it can apparently be taken up quite efficiently by macrophages – a property which, incidentally, has led to its being trialled as an RNA vaccine delivery system – this is a dead end, and one that is quite normal for particles of any kind being introduced into mammals.

Which is something that happens every day, as we and our cousin mammals eat: it has been shown elsewhere that animals are actually quite good spreaders of plant viruses, some of which – like TMV and the even tougher Cauliflower mosaic virus – pass right through at high survival rates, and remain infectious.  We will all probably have eaten many grams of various viruses in our lives, and derived nothing more than nutrition from them.

I also remember, even though it was very late at night, 31 years ago, and in a bar in Banff in Canada, a conversation with one Richard Zeyen.  He told me they had used ELISA to test everyone in their lab for antibodies for TMV, seeing as they worked with it, and had newly developed a test.  And everyone was immune – presumably, to aerosolised TMV that had been breathed in or otherwise ingested.  Proving…that oral vaccines based on TMV could work, and that most of us are probably immune to all sorts of viruses that don’t replicate in us – and nothing more!

Including, in the case of many people in the Eastern Cape Province of South Africa, sampled by one Don Hendry via the local blood bank, to a virus of Pine Emperor moths – because it multiples to such high levels in its host that anyone walking in the pine forests was bound to be exposed via the environment.

So this is an interesting paper – and no more.  It will, of course, lead to alarmist articles and blog posts, and people calling out for urgent surveillance of food, in which people will find many viruses.  And so what?  They have been with us for as long as we have been eating plant-derived food, and have NEVER been associated with any disease, transmissible or otherwise – so my best advice is that we ignore them.

See on www.plosone.org

Polio Virus Spreads From Pakistan to Egypt

3 February, 2013

See on Scoop.itVirology News

Health officials in Egypt and the world are scrambling to prevent an outbreak of polio after poliovirus from Pakistan was discovered in sewage samples collected at two sites in Cairo in December.

Genetic analysis just completed has linked the Egyptian viruses to one that was last seen in Pakistan in September 2012. How it got to Cairo remains unclear, but the genetic evidence suggests that the virus made the long journey sometime in the past 3 months. Egypt has been polio-free since 2004.

Ed Rybicki‘s insight:

It really is too bad that this should happen: while it is to be hoped that virus is being shed by people who are not / will not get sick, and that the population is sufficiently well vaccinated that it will not spread, the fact that there is still uncontrolled spread of wild-type poliovirus is hugely concerning.

See on news.sciencemag.org

Genetically modified tobacco plants produce antibodies to treat rabies

2 February, 2013

See on Scoop.itVirology News

Smoking tobacco is bad for your health, but a genetically altered version of the plant might provide an inexpensive cure for the deadly rabies virus.

Ed Rybicki‘s insight:

Going green…seriously, plants represent an extremely useful alternative production system for many biologicals – and especially for antibodies.  Some day, all monoclonals will be made this way…B-)

See on www.sciencedaily.com


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