Archive for April, 2012

An examination of the bacteriophages and bacteria of the Namib desert

30 April, 2012

See on Scoop.itVirology News and here

“Bacteria and their viruses (called bacteriophages, or phages), have been found in virtually every ecological niche on Earth. Arid regions, including their most extreme form called deserts, represent the single largest ecosystem type on the Earth’s terrestrial surface. The Namib desert is believed to be the oldest (80 million years) desert. We report here an initial analysis of bacteriophages isolated from the Namib desert using a combination of electron microscopy and genomic approaches. The virus-like particles observed by electron microscopy revealed 20 seemingly different phage-like morphologies and sizes belonging to the Myoviridae and Siphoviridae families of tailed phages. Pulsed-field gel electrophoresis revealed a majority of phage genomes of 55-65 kb in length, with genomes of approximately 200, 300, and 350 kb also observable. Sample sequencing of cloned phage DNA fragments revealed that approximately 50% appeared to be of bacterial origin. Of the remaining DNA sequences, approximately 50% displayed no significant match to any sequence in the databases. The majority of the 16S rDNA sequences amplified from DNA extracted from the sand displayed considerable (94-98%) homology to members of the Firmicutes, and in particular to members of the genus Bacillus, though members of the Bacteroidetes, Planctomycetes, Chloroflexi, and delta-Proteobacteria groups were also observed.”

This serves as a neat, if slightly dated, little introduction to my latest endeavour – and an account of a field trip this last week into the Namib Desert.

I was fortunate enough some time ago to have been invited by Don Cowan, presently of University of Pretoria, to accompany his team to the Gobabeb Research and Training Centre inland of Walvis Bay, in Namibia’s Namib Desert.  They work on extremophiles, and the Namib is a great environment for mining bugs that can withstand high salt and temperatures and severe desiccation – oh, and photosynthesise underground, hiding under semi-tranlucent quartz rocks embedded in the surface soil.  The thinking was that, given my long-time interest in viral diversity and newly-acquired means to do oceanic viromics, I would be interested and even of some help.

And so it has come to pass: I will have my very own hypolith (=rock-colonising blue-green algae) scrapings and the result of diafiltration and concentration of washings of a good few kilos of red dune sand to play with as far as virus genome sequencing and even EM and analytical centrifugation go.

Typical quartz-associated hypolith

We will have fun in the coming months…that, and we will obviously HAVE to go back to Gobabeb, to further investigate whatever it is we find.  A terrible, harsh place, but SOMEONE has to go there…B-)

Nothing beside remains...boundless and bare
The lone and level sands stretch far away
PB Shelley, Ozymandias

Env-less endogenous retroviruses are genomic superspreaders

30 April, 2012

See on Scoop.itVirology News

Endogenous retroviruses (ERVs) differ from typical retroviruses in being inherited through the host germline and therefore are a unique combination of pathogen and selfish genetic element. Some ERV lineages proliferate by infecting germline cells, as do typical retroviruses, whereas others lack the env gene required for virions to enter cells and thus behave like retrotransposons. We wished to know what factors determined the relative abundance of different ERV lineages, so we analyzed ERV loci recovered from 38 mammal genomes by in silico screening. By modeling the relationship between proliferation and replication mechanism in detail within one group, the intracisternal A-type particles (IAPs), and performing simple correlations across all ERV lineages, we show that when ERVs lose the env gene their proliferation within that genome is boosted by a factor of ∼30. We also show that ERV abundance follows the Pareto principle or 20/80 rule, with ∼20% of lineages containing 80% of the loci. This rule is observed in many biological systems, including infectious disease epidemics, where commonly ∼20% of the infected individuals are responsible for 80% of onward infection. We thus borrow simple epidemiological and ecological models and show that retrotransposition and loss of env is the trait that leads endogenous retroviruses to becoming genomic superspreaders that take over a significant proportion of their host’s genome.

 

I love it: retroviruses that choose to spread WITHIN a cell’s genome, rather than between cells.  Safe little niche, as long as it keeps dividing!

See on www.pnas.org

CDC: 2011 was worst measles year in US in 15 years – BusinessWeek

21 April, 2012

See on Scoop.itVirology News

“Last year was the worst year for measles in the U.S. in 15 years, health officials said Thursday.

There were 222 cases of measles, a large jump from the 60 or so seen in a typical year. Most of the cases last year were imported — either by foreign visitors or by U.S. residents who picked up the virus overseas.

U.S. children have been getting vaccinated against the measles for about 50 years. But low vaccination rates in Europe and other places resulted in large outbreaks overseas last year.

So far this year, 27 U.S. cases have been reported and it’s too early to gauge whether 2012 will be as bad as last year. But with large international events like the London Olympics coming up, health officials are urging everyone — particularly international travelers — to make sure they’re fully vaccinated.”

 

And so it begins…the collapse of what used to be near-universal anti-measles vaccination, resulting in re-importation of the virus to places where it had almost been eradicated.

See on www.businessweek.com

Vietnam’s new war: Incurable mystery virus [=EV71] kills 19 kids to date — RT

21 April, 2012

See on Scoop.itVirology News

“Hanoi has asked the World Health Organization for help to cure a virulent disease affecting children. Symptoms include blistering on hands, feet and mouths accompanied by high fever and eventual organ failure.

Nineteen children died from the illness in 2011 alone.
The virus spreads through direct contact with an infected person’s oral discharges or saliva, the fluid from burst blisters or the stool of infected persons.
The Red Cross mission in Vietnam reports the disease has already infected over 28,000 children this year, which is more than 10 times the number of infected children in the same period last year.
According to the International Federation of Red Cross and Red Crescent Societies (IFRC), last year a record 110,000 children became infected, with 169 deaths.
The hand, foot and mouth disease (HFMD) disease mostly affects children under three years old (80 per cent of totals cases) the Red Cross said. There is no known treatment for HFMD.”

 

The virus is EV71, a picornavirus similar to the polioviruses and hepatitis A virus – so hardly a “mystery virus”.  There are also a number of vaccines in the pipeline for the disease, including one highlighted here a while ago.

See on rt.com

USUTU VIRUS – POTENTIAL RISK OF HUMAN DISEASE IN EUROPE

21 April, 2012

See on Scoop.itVirology News

Usutu virus (USUV) is an African mosquito-borne flavivirus, member of the Japanese encephalitis antigenic group. This avian virus is transmitted by arthropod vectors (mainly mosquitoes of the Culex pipiens complex). It is well known that free-living birds, including migratory species, have the potential to disperse certain pathogenic microorganisms. Usutu virus has recently been introduced to Europe and is spreading through Austria, Hungary, Italy, Spain and Switzerland, causing disease in birds and humans. Like West Nile virus, USUV may become a resident pathogen in Europe and the consequences for public health should be considered. Many different biotic and abiotic factors affect the survival of the virus in a new environment and influence the efficiency of its geographical dispersal

See on www.eurosurveillance.org

Biology Direct | Abstract | A novel virus genome discovered in an extreme environment suggests recombination between unrelated groups of RNA and DNA viruses

20 April, 2012

See on Scoop.itVirology News

“Viruses are known to be the most abundant organisms on earth, yet little is known about their collective origin and evolutionary history.  With exceptionally high rates of genetic mutation and mosaicism, it is not currently possible to resolve deep evolutionary histories of the known major virus groups. Metagenomics offers a potential means of establishing a more comprehensive view of viral evolution as vast amounts of new sequence data becomes available for comparative analysis.

Bioinformatic analysis of viral metagenomic sequences derived from a hot, acidic lake revealed a circular, putatively single-stranded DNA virus encoding a major capsid protein similar to those found only in single-stranded RNA viruses. The presence and circular configuration of the complete virus genome was confirmed by inverse PCR amplification from native DNA extracted from lake sediment. The virus genome appears to be the result of a RNA-DNA recombination event between two ostensibly unrelated virus groups.”

Not the first time this is postulated to have happened, although the authors have cited the first one: Gibbs and Weiller, 1999.

See on www.biology-direct.com

Engineered H5N1: the wheels grind on, and on, and on….

19 April, 2012

The Scientist has a nice collection of articles on this topic, which I have commented on all over the place, so I though I might consolidate some of it in one place.

In response to the article entitled “Deliberating Over Danger“, I wrote the following:

The point I and others have made before is that H5N1 and other influenza viruses are not waiting for us to let engineered versions loose, before they cause pandemics: all of the mutations noted by the Fouchier and Kawaoka groups are almost certainly present in the several environments where H5N1 viruses are now endemic – and all it takes for all of them to be present together is a little more mixing.

Don’t discount other flu subtypes, either: while everyone is obsessing about H5N1, H3N2 is busy popping out of pigs in the USA; H9N2 in birds in Bangladesh; H5N2 in ostriches in South Africa – and all it would take is one or a couple of fortuitous reassortments, and a whole new flu virus could be unleashed.

While the “deadly” H5N1s are being worked on in lockdown facilities.

If we don’t know what the virus does, we won’t know what it can do. If we don’t know what to look for, we may be taken unawares, when the next 1918-type pandemic strikes.

I want to have universal flu vaccines by then – so we won’t HAVE to worry about a new flu

.

There are also three newer articles covering the controversy: these are

  • H5N1 Researcher to Defy Dutch Gov’t?
  • (with my comment – “Export permit to publish something?  Really?  A complete misapplication of laws to material that should not be subject to them.”)
  • White House Weighs in on H5N1
  • Flu Review Criticized
  • (with my comment – “So after a full and frank hearing did not go his way, after changes had been made to the paper in question (Fouchier’s), Osterholm complains.  Such is life….”

There is the slightly older article – “Bird Flu Papers to Publish” - describing the reversal of the NSABB’s decision to ask for redaction of the two papers describing mammal-to-mammal aerosol-transmissible H5N1.

An interesting article also describes Yoshihiro Kawaoka’s results:

“First, he introduced two mutations—N224K and Q226L—into the haemagglutinin (HA) protein of H5N1 that made the virus capable of sticking to receptors on human tracheal cells. Then he created a chimeric virus by combining the mutated HA protein with genes from the H1N1 virus, which sparked a pandemic in 2009. Kawaoka identified another HA mutation, called N158D, that allowed the virus to spread between ferrets that were not in direct physical contact. A fourth mutation, T318I, also showed up in the H5N1 strain, but its role in making the virus more transmissible among mammals is less clear.”

So there you are: an actual recipe for aerosol-transmissible H5N1.  It was always going to come out somehow, and now these two papers will probably the most cited flu papers ever.  Nothing like a little hype!  Meanwhile, H5 and its brothers and sisters are out there mutating away, with no help needed from anyone.  Roll on universal flu vaccines!!

Russell Kightley’s Scientific Illustration Blog: Influenza Virus Structure Animation

19 April, 2012

See on Scoop.itVirology News

“I have just created an animation of a rotating influenza virus. The sequence begins with a still of the cutaway virus with various parts labelled. The labels disappear and the virus rotates, then returns to the starting graphic. This is in high definition and looks good full screen on a 27″ iMac. It is the latest addition to my YouTube Channel.”

 

Definitely, graphics courtesy of Russell Kightley Media…B-)  STRONGLY commended!

See on blog.kightleys.com

From herd immunity and complacency to group panic: How vaccine scares unfold

19 April, 2012

See on Scoop.itVirology News

A new study, published in PLoS Computational Biology, shows how worries over vaccine risks can allow preventable contagious diseases, such as measles and whooping cough, to make a comeback.

 

I remember commenting, some 17 years ago, that people in Kikwit should be more concerned than people in the urban USA about Ebola risks from the outbreak then occurring – but probably weren’t, largely because they knew that spread required contact, AND they had no internet to spread the panic.  Virally…in fact, one correspondent coined the term “Ebola Preston” to account for the fear-of-virus propagated by Richard Preston, whose book “The Hot Zone” piggy-backed the Ebola epidemic to huge sales.

 

The bottom line is that people who obsess about safety of vaccines are the ones who are themselves almost certainly protected because THEIR parents followed public health guidleines – but they will be opening their kids up to all of the old scourges that they themselves were protected against.

 

Because they are functionally STUPID.

See on www.eurekalert.org

Heterologous RNA silencing suppressors from both plant- and animal-infecting viruses support Plum pox virus infection

19 April, 2012

See on Scoop.itVirology News

“HCPro, the RNA silencing suppressor (RSS) of viruses belonging to the Potyvirus genus in the Potyviridae family, is a multifunctional protein presumably involved in all essential steps of the viral infection cycle. Recent studies have shown that Plum pox potyvirus (PPV) HCPro can be successfully replaced by Cucumber vein yellowing ipomovirus P1b, a sequence unrelated RSS from a virus of the same family. In order to gain insight into the requirement of a particular RSS to establish a successful potyviral infection, we tested the ability of different heterologous RSSs from both plant- and animal-infecting viruses to substitute HCPro. Making use of engineered PPV chimeras, we show that PPV HCPro can be functionally replaced by some, but not all, unrelated RSSs, including the NS1 protein of the mammalian-infecting Influenza A virus.”

 

Fascinating stuff: shows how promiscuois, or possibly how universal, the machinery for avoiding silencing is – and how funadamental to the life cycles of viruses.  One could almost argue “virus altruism”?

See on vir.sgmjournals.org


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