Archive for July, 2013

Moratorium on using live rinderpest virus lifted for approved research

30 July, 2013

See on Scoop.itVirology News

Benefits of future research should be carefully balanced against potential risks

Paris, 10 July 2013 – A moratorium on using live rinderpest virus for approved research has been lifted by the Food and Agriculture Organization of the United Nations and the World Organisation for Animal Health (OIE).

The moratorium followed the adoption of a Resolution in May 2011 by all OIE Member Countries that urged members to forbid the manipulation of rinderpest virus containing material unless approved by the Veterinary Authority and by FAO and OIE.

The two organizations have now put in place strict criteria and procedures to follow in order to obtain official approval for any research proposals using rinderpest virus and rinderpest virus-containing materials. One of the most crucial requirements is that the research should have significant potential to improve food security by reducing the risk of a reoccurrence of the disease. This procedure replaces an earlier complete ban on handling the virus.

Rinderpest was formally declared eradicated in 2011, but stocks of rinderpest virus continue to exist in laboratories. In June 2012, a moratorium on handling the virus was imposed after an FAO-OIE survey found that the virus continues to be held in more than 40 laboratories worldwide, in some cases under inadequate levels of biosecurity and biosafety.

When rinderpest was officially eradicated, FAO and OIE member countries committed themselves to forbid the manipulation of rinderpest virus-containing material unless approved by the national veterinary authority as well as by FAO and OIE.

Paramyxovirus EM courtesy of Linda Stannard

Thanks to Len Bracher for alerting me to this.

Ed Rybicki‘s insight:

This is an interesting sequel to the eradication of wild rinderpest virus, which I have covered in some detail here on ViroBlogy: see here ( and here (

The article covers an interesting prospect: that it may be possible to use attenuated, safe vaccines against the related peste des petits ruminants virus (PPRV) not only to protect against any resurgence of rinderpest, but also to eradicate this rather nasty virus.

Which is, apparently, spreading at rather an alarming rate, and is an obstacle to small ruminant production (

So maybe this is “Now for Number 4!” time.

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H5N1 vaccines in humans

24 July, 2013

See on Scoop.itVirology News



2 Doses of unadjuvanted vaccine are necessary to elicit robust antibody titers.

Oil-in-water adjuvants permit antigen sparing.

Antibody titers decline rapidly but can be boosted with additional doses of vaccine.

High titers of antibody are associated with cross-reactivity against other clades.

Prime-boost strategies elicit a robust immune response.




Ed Rybicki‘s insight:

Thanks @MicrobeTweets!

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Antibiotic treatment expands the resistance reservoir and ecological network of the phage metagenome

24 July, 2013

See on Scoop.itVirology News

The mammalian gut ecosystem has considerable influence on host physiology1, 2, 3, 4, but the mechanisms that sustain this complex environment in the face of different stresses remain obscure. Perturbations to the gut ecosystem, such as through antibiotic treatment or diet, are at present interpreted at the level of bacterial phylogeny5, 6, 7. Less is known about the contributions of the abundant population of phages to this ecological network. Here we explore the phageome as a potential genetic reservoir for bacterial adaptation by sequencing murine faecal phage populations following antibiotic perturbation. We show that antibiotic treatment leads to the enrichment of phage-encoded genes that confer resistance via disparate mechanisms to the administered drug, as well as genes that confer resistance to antibiotics unrelated to the administered drug, and we demonstrate experimentally that phages from treated mice provide aerobically cultured naive microbiota with increased resistance. Systems-wide analyses uncovered post-treatment phage-encoded processes related to host colonization and growth adaptation, indicating that the phageome becomes broadly enriched for functionally beneficial genes under stress-related conditions. We also show that antibiotic treatment expands the interactions between phage and bacterial species, leading to a more highly connected phage–bacterial network for gene exchange. Our work implicates the phageome in the emergence of multidrug resistance, and indicates that the adaptive capacity of the phageome may represent a community-based mechanism for protecting the gut microflora, preserving its functional robustness during antibiotic stress.

  T4 phage graphic by Russell Kightley Media

Ed Rybicki‘s insight:

This is a fascinating finding, for a number of reasons: however, most importantly it means that the "phageome" – or bacterial virus metagenome in your gut – is a reservoir of genes that can confer survival advantage(s) on your microbial population when this population is stressed.

For example, by antibiotic therapy.

This alters our concept and understanding of phage-bacteria interactions quite significantly, as it can no longer be understood as a simple "predator/prey" relationship.  Rather, and while phages still regulate bacterial numbers by simply killing them, they also act as stewards or gamekeepers, by making it possible for bacteria to survive adverse events.

Quite a concept that: the virus as conserver!

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Close Relative of Human Middle East Respiratory Syndrome Coronavirus in Bat, South Africa

24 July, 2013

See on Scoop.itVirology and Bioinformatics from

The severe acute respiratory syndrome (SARS) outbreak of 2002–03 and the subsequent implication of bats as reservoir hosts of the causative agent, a coronavirus (CoV), prompted numerous studies of bats and the viruses they harbor. A novel clade 2c betacoronavirus, termed Middle East respiratory syndrome (MERS)–CoV, was recently identified as the causative agent of a severe respiratory disease that is mainly affecting humans on the Arabian Peninsula (1). Extending on previous work (2), we described European Pipistrellus bat–derived CoVs that are closely related to MERS-CoV (3). We now report the identification of a South Africa bat derived CoV that has an even closer phylogenetic relationship with MERS-CoV.


Coronavirus graphic courtesy of Russell Kightley Media

Ed Rybicki‘s insight:

This is interesting and timely work – for which notice, thanks Stephen Korsman! – out of various labs in South Africa and elsewhere.

This almost certainly means that, as with paramyxoviruses in bats, there are a LOT of CoVs out there with the potential to infect other mammals – including humans.

Of course, this one should be the REAL SARSCoV – for "South African respiratory syndrome virus.  Which would make all teh jokes about the SA Revenue Services even more pointed.

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Medical Virology of Hepatitis B: how it began and where we are now?

23 July, 2013

See on Scoop.itVirology News

Infection with hepatitis B virus (HBV) may lead to acute or chronic hepatitis. HBV infections were previously much more frequent but there are still 240 million chronic HBV carriers today and ca. 620,000 die per year from the late sequelae liver cirrhosis or hepatocellular carcinoma. Hepatitis B was recognized as a disease in ancient times, but its etiologic agent was only recently identified. The first clue in unraveling this mystery was the discovery of an enigmatic serum protein named Australia antigen 50 years ago by Baruch Blumberg. Some years later this was recognized to be the HBV surface antigen (HBsAg). Detection of HBsAg allowed for the first time screening of inapparently infected blood donors for a dangerous pathogen. The need to diagnose clinically silent HBV infections was a strong driving force in the development of modern virus diagnostics. HBsAg was the first infection marker to be assayed with a highly sensitive radio immune assay. HBV itself was among the first viruses to be detected by assay of its DNA genome and IgM antibodies against the HBV core antigen were the first to be selectively detected by the anti-mu capture assay. The cloning and sequencing of the HBV genome in 1978 paved the way to understand the viral life cycle, and allowed development of efficient vaccines and drugs. Today’s hepatitis B vaccine was the first vaccine produced by gene technology. Among the problems that still remain today are the inability to achieve a complete cure of chronic HBV infections, the recognition of occult HBV infections, their potential reactivation and the incomplete protection against escape mutants and heterologous HBV genotypes by HBV vaccines.


Ed Rybicki‘s insight:

Not only "…the first vaccine produced by gene technology", but the first virus-like particle vaccine, and the first anti-cancer vaccine.

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Giant Pandoravirus is 1,000 times larger than influenca virus and contains 2556 genes

19 July, 2013

See on Scoop.itVirology News

Giant viruses turn out to be everywhere. It was the very giant-ness of giant viruses that allowed them to be overlooked for so long. Scientists first discovered viruses in the late 1800s when they were puzzled by a disease that beset tobacco plants. They mashed up wilted tobacco leaves with water and passed the mixture through fine porcelain filters that trapped bacteria and fungi. The clear liquid could still make healthy tobacco leaves sick. The Dutch botanist Martinus Beijerinck dubbed it “a contagious living fluid.”


In the 1930s, the invention of powerful microscopes finally allowed scientists to see viruses. They found that viruses were unlike ordinary cells: they didn’t generate their own fuel; they didn’t grow or divide. Instead, viruses invaded cells, hijacking their biochemistry to make new copies of themselves. Being small and simple seemed like part of the viral way of life, allowing them to replicate fast.


It wasn’t until 2003 that a team of French researchers discovered the first giant virus. They had been puzzling over sphere-shaped objects that were the size of bacteria but contained no bacterial DNA. Eventually they realized that they were looking at a monstrously oversized virus, containing 979 genes, much less than the newly discovered Pandoravirus.


Those first giant viruses were isolated from amoebae living in water from a cooling tower. Once scientists realized that viruses could be so large, they changed their search parameters and started finding other species in all manner of places, from swamps to rivers to contact lens fluid.


And along the way the biggest viruses got bigger. In 2011, Dr. Claverie and his colleagues set a new record with megaviruses, a type of giant virus with 1,120 genes they discovered in sea water off the coast of Chile. They then dug into the sediment below that sea water and discovered pandoravirsues, with more than twice as many genes.


Dr. Claverie speculates that pandoraviruses and other giant viruses evolved from free-living microbes that branched off from other life several billion years ago. “The type of cells they may have evolved from may have disappeared,” he said.


The idea that giant viruses represent separate branches on the tree of life is a controversial one that many other experts aren’t ready to embrace. “They provide no evidence for that notion, so it seems a distraction to me,” said T. Martin Embley, a professor of evolutionary molecular biology at Newcastle University.


Despite those reservations, Dr. Embley and other researchers hail pandoraviruses as an important discovery. “I think it’s wonderful that such crazy and divergent lifeforms continue to be discovered,” said Tom Williams, Dr. Embley’s colleague at Newcastle University.


The new study also drives home the fact that giant viruses are far from rare. Shortly after discovering pandoraviruses in sea floor sediment, Dr. Claverie and his colleagues found them in water from a lake in Australia, 10,000 miles away. “It definitely indicates that they must not be rare at all,” said Dr. Claverie.


Giant viruses may be so common, in fact, that they may be hiding inside of us, too. In a paper published online on July 2 in The Journal of Infectious Diseases, French researchers offered evidence that giant viruses dwell in healthy people. They isolated a new giant virus from blood donated by a healthy volunteer, and then found antibodies and other signs of the virus in four other donors.


Giant viruses may lurk harmlessly in our bodies, invading the amoebae we harbor. Whether they can make us sick is an open question. “I don’t believe we have the proof at the moment that these viruses could infect humans,” said Dr. Claverie.

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Man, the taurine excreta just keeps coming….

18 July, 2013

See on Scoop.itVirology News

CDC Admits 98 Million Americans Received Polio Vaccine In An 8-Year Span When It Was Contaminated With Cancer Virus

Ed Rybicki‘s insight:

Two comments I made to this piece:

Unbelievable conflation of facts / pseudofacts / nonsense to come up with "evidence" for a conspiracy!

For your info, PCR – Polymerase Chain Reaction, and amplifies DNA, not protein.

As for "Additional tests were performed for Epstein-Barr virus capside and Cytomeglia virus which are used in bioengineering for gene delivery systems through viral protein envelope and adenoviral protein envelope technology. The individual was positive for both; indicating a highly probable exposure to a DNA vaccination delivery system through nasal inhalation.":

Epstein-Barr virus is NOT used for any human purpose; neither is "Cytomeglia" [sic – actually Cytomegalovirus] – but a very high proportion of the human race is naturally infected with one or both. So how the "evidence" indicates an exposure to a DNA vaccination delivery system, I do not understand.


"SV40 is well known cancer causing virus": in? Experimental animals, yes. Humans? No proof, sorry!

The fact is, if I can so easily poke holes in the tail end of the piece, I see no reason to take the rest of it seriously. I teach Virology: I have known about the SV40 in poliovirus vaccines for more than 20 years; it was never kept secret. But did it ever do any harm? Not that anyone has conclusively been able to show, sorry!

As for "SV40 virus has been found in certain types of cancer in humans.": so have many things. Cancer tissue may be infected adventitiously with all sorts of bacteria and viruses; the history of looking for viral causes of cancers is littered with false correlations. For example, people were convinced that cervical cancers were positively correlated with a herpesvirus – until it was found that human papillomaviruses were the ACTUAL cause. All sorts of claims were made about retroviruses and human breast cancer, but none of them have stuck, despite mouse mammary tumour virus being such a good model system.

Thus, while it is a sad fact of of the history of vaccinology that well-meaning researchers managed to contaminate early poliovirus vaccines with live SV40, there STILL has not been any REAL correlation of its presence with a significant elevation in human cancers. None: and I teach the subject, and I’ve looked into it thoroughly.

Now, how about those pesky porcine circoviruses in the human rotavirus vaccines…? I work on both, so I’d be interested to see what conspiracies could be concocted around THAT. See here for my take:

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WHO: Treat people with HIV early to stop disease’s spread

1 July, 2013

See on Scoop.itVirology News

Young children and certain other people with the AIDS virus should be started on medicines as soon as they are diagnosed, the World Health Organization says in new guidelines that also recommend earlier treatment for adults.

Ed Rybicki‘s insight:

…if it can be afforded…South Africa currently has the world’s largest number of people in any one country on ARVs; 1.7 million out of 6 million infected, in a population of 48-odd million.  Treating more people is effectively unsustainable – which is what would have to happen with these guidelines!

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