Announcement

**gsgs** · April 22, 2013, 10:28 AM

Re: Man Made H5N1 - Super Version

Scientists seek ethics review of H5N1 gain-of-function research

http://www.cidrap.umn.edu/cidrap/content/influenza/avianflu/news/mar2913ethics.html

Presidential Commission for the Study of Bioethical Issues (PCSBI).
acknowledged that the commission received the FVR's request but
declined to comment on it further.
The letter says that more gain-of-function studies on H5N1 and other viruses
are on the way. A Chinese group is working with H5N1, and a Dutch group is
expanding its H5N1 studies to include work with the H7N7 avian flu virus and
has plans for similar research with the SARS coronavirus.
(and now they got H7N9 ....)
Also, German
scientists recently did experiments to see what it would take for canine
distemper virus to spread from dogs to humans, the letter states.

**gsgs** · April 26, 2013, 01:53 AM

Re: Man Made H5N1 - Super Version

CIDRAP Robert Roos wrote at

Page not found | CIDRAP

http://www.cidrap.umn.edu/cidrap/content/influenza/avianflu/news/apr2513receptor.html

> Study: Lab-derived H5N1 virus component binds to human receptors
same Kawaoka-ferret-group as in 2012
> A new study suggests that a lab-derived hybrid H5N1 influenza virus that is
> capable of airborne transmission among ferrets may well be capable of doing
> the same thing in humans.
> ... In some ways, they said, the properties of the mutant HA "suggest that H5 viruses
> could take a similar evolutionary pathway in humans to that followed in 1957 and
> 1968 by avian H2 and H3 viruses.
> ...However, the fact that the mutant virus sacrifices its avian binding ability to gain its
> human affinity "distinguishes it from known pandemic viruses

Racanielli wrote:
> the study offers important contributions but receptor binding is not the only factor
> that determines a flu virus's ability to infect and spread among ferrets and humans.
> the authors find that there is a limit on how many HA?sialic acid interactions can
> occur with one virus particle, and that this explains how modest decreases in the
> dissociation constant [the strength of single HA-receptor interactions] (~15-fold)
> can lead to a complete loss of binding and the resulting effects on receptor specificity.
> I think this is an important contribution which unifies the physical measurements with
> the ability of viruses to infect cells.
> To summarize the important contributions of this work, the ferret transmissible HA
> has a small increase in affinity for human receptors and a large decrease for avian
> receptors; alpha-2,6 sialic acid binds this HA in a way typical of human pandemic
> strains, and different from how wild-type H5 binds avian sialic acids.
> They [the authors] suggest that the transmissible H5 would not arise in waterfowl,
> given its lack of binding to avian receptors. These data help guide analysis of viral
> sequences for pandemic potential, and make important links between HA sequences,
> structure, and receptor binding.
> However, it is important to remember that aerosol transmission is far more complex
> than just being able to bind a receptor, and involves other parameters such as efficient
> shed from cells, the ability to replicate, stability, and probably others. For humans,
> the nature of those other changes is unknown.

Wain-Hobson, wrote:
> I express alarm over the findings.
> What I conclude here is that this virus does bind the sugar receptor as would a
> mammalian virus, in which case, as we know it goes from ferret to ferret, it's very
> reasonable to assume this is a novel human virus. The world is a more dangerous place.
> the report says that the virus will replicate in the upper respiratory tract due to affinity
> for the alpha2,6-linked sialic acids?just like any good mammalian influenza virus.
> It also says that as the virus has lost its binding for alpha2,3-linked sialic acids it won't
> get stuck on the mucin surfaces in the airways.
> This means that airborne virus will get down to the upper respiratory tract almost unhindered.
> So it will get into the right place and it will replicate. And because it won't get stuck on the
> mucin, it will get out.
> if Kawaoka's (or Fouchier's) virus escaped from a lab, it might not become a pandemic
> strain immediately, but it could begin spreading in humans and quickly evolve into one.
> So even if this Kawaoka configuration isn't the BIG ONE, it could rapidly lead to it,

**Sally Furniss** · April 26, 2013, 02:09 AM

Re: Man Made H5N1 - Super Version

<table border="0" cellpadding="0" cellspacing="6" width="100%"><tbody><tr><td class="alt2"></td> <td nowrap="nowrap"> Shiloh
Editor, Senior Moderator
</td> <td width="100%"> </td> <td nowrap="nowrap" valign="top"> Join Date: Feb 2008
Posts: 29,275

</td> </tr> </tbody></table> Re: Man Made H5N1 - Super Version
<hr style="color:#CCCCCC; background-color:#CCCCCC" size="1"> Source: http://www.businessweek.com/news/201...haracteristics

Mutant Bird Flu Virus Evolves to Show Pandemic Characteristics
By Makiko Kitamura
April 24, 2013

A mutant version of a bird flu virus created by scientists last year to show its ability to spread between humans evolved to show characteristics of previous pandemic viruses, a study found.

A genetic component of the mutant H5N1 virus developed a 200-fold preference for binding with human over avian receptors, according to a study led by researchers at the MRC National Institute for Medical Research in London. Their paper was published today in the scientific journal Nature.

The study builds on work led by Yoshihiro Kawaoka at the University of Wisconsin-Madison that showed how H5N1 could become highly transmissible if its hemagglutinin gene is mutated and mixed with those of the H1N1 virus that sparked the 2009 swine flu pandemic. As a follow-up, the MRC-led team plans to study the same binding properties of the current H7N9 virus reported in China, John Skehel, one of the study authors in London, said in a phone interview...

**gsgs** · April 26, 2013, 02:15 AM

Re: Man Made H5N1 - Super Version

As I understand, Racaniello thinks,
that this is an important step in our understanding how to create a devastating pandemic.
But also that the approach is not sufficient yet and that fundamentally new approaches
are needed to complete the task. Mainly because we have only ferret experiments,
so what's needed for humans is unknown.
----------------------------
Now, there are ethical problems with human experiments, but even without these,
they are more and more successful to research around it, find other ways
and I feel that we are close to creating pandemic viruses with lots of new antigenic profiles.
Adapting the virulence of these should be the easier task.
So, should we prepare to let mild versions lose on mankind should someone else
let lose an antinically similar virulent variant ?
So to induce immunity against the evil one by real infections, which still seems to be
more effective then vaccinations.

But I also see the potential of vastly increased different pandemic candidates.
They might be able soon to create many antigenically different HAs, not just
limited to the existing 17 types.and their naturally occurring subtypes.
Once we undestand this, we can "design" many new HA-types and create them
by increased evolution, mutating,selecting,computer simulation,
microscale thermophoresis,surface biolayer interferometry,...(we are just at the beginning)

Then we will have lots of new pandemic candidates and lots of vaccines and antivirals too.
But I feel that constructing new pandemic candidates will be easier than creating
countermeasures against them.

------------------------------------------------
I think they should have addressed this dual-use concern in the paper.
They talk about the possible benefits and importance of their work a lot,
but leave out the risks, although they are clearly aware of that discussion.
That makes the thing incomplete, even somehow unscientific and similar
to a biased advertisement for their work.
-----------------------------------------------------------------

you can read through the first 6 of the 11 pages (plus references) with some reading tool, "readcube"
but not print or download it.

303 See Other

http://www.nature.com/nature/journal/vaop/ncurrent/full/nature12144.html

"preview"

Receptor binding by a ferret-transmissible H5 avian influenza virus

http://www.readcube.com/articles/10.1038/nature12144?utm_campaign=readcube_access&utm_source=nature.com&utm_medium=purchase_option&utm_content=thumb_version

you can purchase the article for $30, but have to agree to some lengthy terms and conditions,
which presumably includes that you maynot quote and discuss it here (?)

---------------------------------------------------------------

**gsgs** · May 14, 2013, 02:55 AM

Re: Man Made H5N1 - Super Version

Just a moment...

http://news.sciencemag.org/sciencenow/2013/05/gene-swap-helps-bird-flu-spread-.html

> They then took the most pathogenic hybrids—based on tests in mice—and gauged
> whether these composite viruses would transmit between guinea pigs

Mix-and-match. Chen Hualan
Yoshihiro Kawaoka
Fouchier's group
Wendy Barclay,

Barclay says she expects more gain-of-function studies will help clarify just
what ingredients H5N1 needs to become a pandemic virus.

Ebright : http://chem.rutgers.edu/ebright_richard_h
> expanding the line of research is risky.

Wain-Hobson:
> the new study—although of high quality—is very dangerous work.
> One wonders why it is published in Science

Fears for man-made bird flu bug

http://dawn.com/2013/05/03/fears-for-man-made-bird-flu-bug/

Scientists in China have created a hybrid bird flu virus that can spread in the air

================================================== ===========================

[ discussion from
http://www.virology.ws/2013/05/07/in...-good-science/ ]
[ I also put it here :

http://gsgs2.blogspot.de/2013/05/man-made-pandemics.html

and here:
[FT]

for better formatting and possible later editing and additions and graphics
and responses and discussion ]

--------------------------------------------------------------------------------------------------------

profvrr wrote on 2013.May.13 in response to DavidS

> Animal models are not predictors of what will happen in humans.

somehow they are.That's why we are using them, why you say "it's good science"
You probably meant: are not so good predictors (as most think)

> We study infections in animals to obtain mechanistic clues;

you say mechanistic clues, I'd say probability estimates

> conclusions about what happens in people require further testing. There are dozens
> of examples of this in the literature. Drugs and vaccines are tested in several animal models,
> but are the drugs and vaccines then released for humans? Of course not; clinical
> trials are done.

which often however confirm the animal tests. I'd guess in ~70% of cases

> We've had a great deal of experience in this laboratory constructing viruses with
> various mutations, and none have ever been more virulent; most are attenuated.
> The same applies for research done in other laboratories. We have little clue how
> to make a more virulent virus.

but there are many papers demonstrating just this increase of virulence.
I don't know much outside influenza, but especially with reassorting influenza viruses :
we have 256 possible children, some are usually
more virulent than the parents, some are less virulent. Only ~10% do survive and replicate
and most transmit worse than in nature. But now I feel that we are getting close to successfully
create/detect and filter the potential candidates. We are clearly better than nature here,
which requires a (rare in humans) double-infection and competition (through immunity) with other viruses,
while we can learn and design and select to specifically target and optimize the outcome.
Since above study is not public and already starts with a HP-virus,
let me select this as an example instead, to demonstrate what I mean Sun et.al., 2011:

Just a moment...

http://www.pnas.org/content/early/2011/02/23/1019109108

[ For an overview of other reassortment studies see
http://www.flutrackers.com/forum/sho...d.php?t=203696 ]
While most (46 out of 127) [H9N2+pH1N1)-reassortant viable children had lower pathogenicity
than the parents, there were still 8 out of 127 that had higher pathogenicity in mice than both
parents.Researchers and terrorists will learn how to create higher pathogenicity by reassortment
or passaging or combinations of both. And how to enhance it to ferrets,pigs,...,humans.

This was for reassortment experiments, but also for single mutations and passaging
there are many papers how these may increase virulence.
Some keywords that come to mind:: N66S in PB1-F2, E627K in PB2, H5N1 in mouse-brain
after passaging, chicken-adapted,quail-adapted H9N2, D225G in HA of pH1N1 and 1918-H1N1,
search "virulence mutations", "influenza"

> Part of the problem is that we focus on amino acid
> changes in isolation; in nature these are accompanied by hundreds of other changes
> which are eventually selected in various hosts to make the final pathogen.

in flu it's often just one mutation. And the mutations usually accumulate one by one.
Each of the viruses in that chain must be viable. We have many influenza sequences
meanwhile, so we can study the chains. And in the labs they can create these mutations
by passaging.

> We don't have a chance at duplicating this and I've never seen any laboratory come close.

Palese,Fouchier,Kawaka,...I feel they are pretty close

> Just take a look at the scientific literature on viral pathogenesis.
> My beliefs are indeed relevant. They are based on 30+ years of doing research in the
> laboratory on viral pathogenesis, and keeping up with the literature.

but things have changed a lot recently. Now we have reverse genetics, better organized
labs with rooms full of ferret-cages, 200000 flu sequences at genbank, 70000 flu-papers at pubmed.
Next Generation Sequencing

---------------------------------------------------------------------------------------------------------------------------

profvrr wrote:
> I firmly believe that laboratory-constructed viruses do not have what it
> takes to be a human pathogen: only viral evolution in nature can
> produce the right combination of RNA segments and mutations.
> ... I can find plenty of virologists who would have the same view.
> We are talking about humans, not animal models.

laboratory-constructed viruses do have what it takes to be a ferret pathogen ?
Humans are animals. We are not so special from the virus' POV.
Why might it work in different animals but not in humans ?
Presumably only because we can't test it in humans for ethical reasons.
There is no magical difference that separates humans from ferrets
but not ferrets from mice or guinea pigs. We cannot be 100% sure
before we tested it in humans - but maybe 80%, and that's still useful.
So lab-viruses probably often do have "what it takes to be an animal or
human pathogen" but tests to confirm this for humans are rarely available.

----------------------------------------------

Evidence of Expanded Host Range and Mammalian-Associated Genetic Changes in a Duck H9N2 Influenza Virus Following Adaptation in Quail and Chickens

http://www.plosone.org/article/info:doi/10.1371/journal.pone.0003170

H9N2 avian influenza viruses continue to circulate worldwide; in Asia, H9N2 viruses have caused disease outbreaks and established lineages in land-based poultry. Some H9N2 strains are considered potentially pandemic because they have infected humans causing mild respiratory disease. In addition, some of these H9N2 strains replicate efficiently in mice without prior adaptation suggesting that H9N2 strains are expanding their host range. In order to understand the molecular basis of the interspecies transmission of H9N2 viruses, we adapted in the laboratory a wildtype duck H9N2 virus, influenza A/duck/Hong Kong/702/79 (WT702) virus, in quail and chickens through serial lung passages. We carried out comparative analysis of the replication and transmission in quail and chickens of WT702 and the viruses obtained after 23 serial passages in quail (QA23) followed by 10 serial passages in chickens (QA23CkA10). Although the WT702 virus can replicate and transmit in quail, it replicates poorly and does not transmit in chickens. In contrast, the QA23CkA10 virus was very efficient at replicating and transmitting in quail and chickens. Nucleotide sequence analysis of the QA23 and QA23CkA10 viruses compared to the WT702 virus indicated several nucleotide substitutions resulting in amino acid changes within the surface and internal proteins. In addition, a 21-amino acid deletion was found in the stalk of the NA protein of the QA23 virus and was maintained without further modification in the QA23CkA10 adapted virus. More importantly, both the QA23 and the QA23CkA10 viruses, unlike the WT702 virus, were able to readily infect mice, produce a large-plaque phenotype, showed faster replication kinetics in tissue culture, and resulted in the quick selection of the K627 amino acid mammalian-associated signature in PB2. These results are in agreement with the notion that adaptation of H9 viruses to land-based birds can lead to strains with expanded host range.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC347656/ 1982
10 avian strains in squirrel monkeys and hamsters

Mouse-adapted H9N2 influenza A virus PB2 protein M147L and E627K mutations
are critical for high virulence

http://jvi.asm.org/content/77/6/3816.full H5N1,mousebrain,2001
all five genotypes of the H5N1/01 viruses were of low pathogenicity in mice
(MB variants) were isolated from the brain by culturing virus-positive brain homogenate
in 10-day-old embryonated hens' eggs for one passage.
The MB variants ... were markedly more virulent than the original viruses

**gsgs** · June 19, 2013, 12:48 AM

Re: Man Made H5N1 - Super Version

they got enhanced translation, although the new virus was not yet
(much) more virulent:

403

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2754401/

this is polio, not influenza, but they used the same method for influenza too.
(link to the 2013-paper)
But only the "Min" variant, they don't mention whether they also tested
the flu-Max and how it behaved. You can easily imagine to make flus
more virulent this way, while polio is already virulent, not much to
"gain" there.

> In contrast, PV-Max P1 produced more F-Luc per unit of R-Luc than did the wild type,
> consistent with enhanced translation (Fig. 2B).
>... PV-SD, with 937 mutations in synonymous codons in the P1 region (5). In PV-SD,
> neither codon bias nor codon pair bias was changed, and that virus was not attenuated

>... It is noteworthy that even though PV-Max
> contains overrepresented codons, it is not more virulent than the wild type (Table 1),
> possibly because evolution has already effectively optimized encoding.

or possibly because they specifically chose one PV-Max that was not more virulent
while rejecting all those that were. So to get the paper through NSABB.

So, now we have (at least) 4 methods to make viruses more pandemiclike and/or adapt them to humans
1.) reassortment
2.) inducing known mutations that confer receptor-specifity, stability,temperature adaption
see Fouchier,Kawaoka
3.) passaging , see Fouchier
4.) codon (-pair) optimization , see Wimmer

through a suitable combination and choice of the starting viruses, it should be
possible or even likely to create pandemic viruses.
Much better and faster than nature could ever do it....

Maybe they already have it
Maybe we need to wait for some lab-worker to talk to a newspaper
about it while seeking asylum in a H5-country, where they
better understand the concern.

-----------------------------------------------
in Coleman's thesis

http://dspace.sunyconnect.suny.edu/bitstream/handle/1951/45442/000000370.sbu.pdf?sequence=3

(160 pages, .pdf)
there is a chart comparing the growth of PV-max with wildtype virus

he concludes that PV-Max has identical growth, despite the enhanced translation.
"Identical" maybe in logarithmic thinking, but from the chart I conclude, that PV-Max
has still ~1.5 times more titers between hours 5 and 25.
If it were flu, would that be sufficient to outcompete existing strains ?

Codon usage bias - Wikipedia

http://en.wikipedia.org/wiki/Codon_usage_bias

Attached Files

**gsgs** · August 19, 2013, 11:32 PM

Re: Man Made H5N1 - Super Version

in Oct.2005 NSABB decided that the recovered 1918-H1N1
genome should be published.
2 months before I became a flubie and 4 months before flutrackers
was created.

Now I'm looking for their official statement, the reasons that were given.

And, stragely, I couldn't find it online.
Any idea, where to find it ?
Any flubie here who went through that discussion in 2005 ?

It was noted by Fouchier and Imperiale that they only knew about the
existing 1918-antibodies since 2009

----------------------edit-----------------------------------------------------------------------------------
obviously NIH was pro-publishing of the 1918 genome in 2005, see below.
Fauci also published papers with Taubenberger and Morens.

found this:

http://oba.od.nih.gov/biosecurity/meetings/NSABB%20November%202005%20meeting%20minutes%20-%20Final.pdf

A fundamental policy challenge described by Dr. Zerhouni relates to decisions on diffusion of
knowledge. The complexity of this issue was evidenced not long before, when the sequence of
the 1918 influenza virus was published. Dr. Zerhouni said the benefits of making the sequence
available to hundreds of laboratories committed to the good use of life sciences research
outweighed the risks

Mr. Leavitt thanked the Board for their rapid response in reviewing the
manuscripts on the reconstruction of the 1918 influenza virus. He said their advice was
extremely helpful in guiding the actions taken and that the Board will be called upon again in
similar situations.

Dr. Kasper summarized the outcomes of the second meeting of NSABB, which took place in
September of 2005 in a closed session to consider the publication of manuscripts about the
reconstructed 1918 influenza virus. Because the manuscripts were unpublished at the time and
were considered confidential, the Board's deliberations were closed to the public.

discussion page 16

------------------------------------------------

here is the mentioned NAS (National Academy of Sciences) report
"Biotechnology Research in an Age of Terrorism"

122 pages , .pdf

http://www.nap.edu/html/biotechnology_research/0309089778.pdf

(I found nothing about the risk of a recurring 1918-Spainflu in that paper with keyword "1918")

**Pathfinder** · December 21, 2013, 10:17 PM

Re: Man Made H5N1 - Super Version

'Untrue statements' anger over work to make H5N1 bird-flu virus MORE dangerous to humans

Coalition of leading scientists claim ferret experiments could lead to a pandemic

Steve Connor
Science Editor
Friday 20 December 2013
...
More than 50 senior scientists from 14 countries, including three Nobel laureates and several fellows of the Royal Society, have written to the European Commission denouncing claims that the ferret experiments are necessary for the development of new flu vaccines and anti-viral drugs.
...
The letter signed by 56 eminent scientists, many of whom are national science academicians, was designed to correct "misstatements" made by the president of the European Society of Virology, Professor Giorgio Palu, who they claim made "incorrect" assertions about the need to carry out the research in an earlier letter he had sent to the Commission.
...
Professor Palu said that Dr Fouchier's "gain of function" experiments are designed to see what kind of mutations are necessary to enable the bird-flu virus to be transmissible between mammals in order to make better vaccines and drugs, and that these mutations have already been seen in nature.
...
However, the letter from the 56 scientists, including Lord May of Oxford, a former government chief scientist, states that this assertion is wrong and gives a false impression about the medical need to undertake such dangerous research.

"The sole purpose of the experiments in question was to generate H5N1 viruses that could be transmitted between mammals as readily as seasonable flu via respiratory droplets ie coughing and sneezing," the letter says.

"Despite intensive field surveillance conducted by national health authorities, government agencies, local and regional disease surveillance networks in Southeast Asia and elsewhere over a period of 16 years, there is no evidence that efficiently mammalian transmissible H5N1 viruses have ever emerged naturally in the wild," it says.
...
"The potential for accidental release of a hazardous pathogen is real, not hypothetical, as demonstrated by an alarming increase in the number of potential and actual release events in laboratories working with high-threat pathogens," they say.
...
Full text:

'Untrue statements' anger over work to make H5N1 bird-flu virus MORE

http://www.independent.co.uk/news/science/untrue-statements-anger-over-work-to-make-h5n1-birdflu-virus-more-dangerous-to-humans-9018666.html

Coalition of leading scientists claim ferret experiments could lead to a pandemic

**gsgs** · December 22, 2013, 12:48 AM

Re: Man Made H5N1 - Super Version

see also:

303 See Other

http://www.nature.com/news/scientists-call-for-urgent-talks-on-mutant-flu-research-in-europe-1.14429

this FT-page loads slowly for me, shouldn't we make a new thread ?

btw. the FVR website should have been "fully functional" in fall 2013
but is still down, now they say it will be fully functional
in spring 2014

**Laidback Al** · December 22, 2013, 01:29 AM

Re: Man Made H5N1 - Super Version

From the article cited by Pathfinder in post #294 above:

? . . . there is a serious risk of an accidental release of a pandemic H5N1 virus from laboratories undertaking such research.

"The potential for accidental release of a hazardous pathogen is real, not hypothetical, as demonstrated by an alarming increase in the number of potential and actual release events in laboratories working with high-threat pathogens," they say.

"We are in a situation where the probabilities of a laboratory accident that leads to global spread of an escaped mutated virus are small but finite, while the impact of global spread could be catastrophic," they add.

Supporting this point of view is a recent article in BMC Medicine entitled ?Containing the accidental laboratory escape of potential pandemic influenza viruses?. Based on simulations, the authors suggested that a lab escape of a novel infectious disease would not be immediately detected, dependent on the reproductive number of the infection disease. The reproductive number is the number of additional individuals infected from a single case. When the reproduction number is less than 1 the infectious disease will not spread. As the reproductive number increases to greater than 1, there is a greater likelihood that the disease will develop into an epidemic and perhaps a full blown pandemic.

According to the authors, it might be possible to control an epidemic outbreak as long as the reproductive number is less than 1.5. To date, the lack of a human H5N1 epidemic demonstrates that H5N1 has not exceeded a reproductive threshold of 1.0. But that could change in the future with either a lab escape of a modified strain or a wild strain of H5N1.

The article cited by Pathfinder also states:

"Despite intensive field surveillance conducted by national health authorities, government agencies, local and regional disease surveillance networks in Southeast Asia and elsewhere over a period of 16 years, there is no evidence that efficiently mammalian transmissible H5N1 viruses have ever emerged naturally in the wild," it says.

While this statement is true today, it does not mean that a strain of H5N1 cannot become easily transmissible in the wild tomorrow.

Although it is not certain which influenza strain was dominant and circulating before the 1918 H1N1 pandemic outbreak, there is more recent evidence that reassortant influenza strains can quickly supplant existing influenza strains.

The issue is a public health conundrum. Should laboratory experimentation on modified strains of H5N1 continue in order to prepare for a potential H5N1 pandemic, or should public officials avoid the dangers of laboratory experimentation and continue to hope that a wild strain of H5N1 does not become easily transmissible and turn into the next pandemic influenza virus.

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**gsgs** · December 22, 2013, 02:15 AM

Re: Man Made H5N1 - Super Version

I found the letter !

Just a moment...

http://news.sciencemag.org/sites/default/files/media/Letter%20to%20Barroso_0.pdf

they want to organize a "briefing"
> FVR has experience and expertise to organize such a briefing

is it that what FVR mainly does, what their business is ?
I do not see the purpose of a briefing, I have no experience with briefings.
Aren't emails and posts and online papers better,faster,easier than briefings ?

2. they call for a comprehensive risk-benefit assessment on gof-research.

yes, I second that. I'd like to add that it should involve subjective probability
estimates and not only the official gof-research but also the expected
and anticipated secret gof-research

**gsgs** · February 10, 2014, 01:29 PM

Re: Man Made H5N1 - Super Version

http://optionsviii.controlinfluenza.com/conference-materials/

The Pros and Cons of Influenza Gain of Function Studies
CapeTown,Sep.2013 Sat.Sep.7.2013 , 8:00-11:30 Panelists include:
Yoshihiro Kawaoka, University of Wisconsin Madison,
Charles Russell, St. Jude Children’s Research Hospital, Memphis,
Adolfo Garcia-Sastre, Mount Sinai School of Medicine, New York,
Michael Osterholm, Center for Infectious Disease Research and
Marc Lipsitch, Harvard University, Cambridge, Massachusetts,
Jesse Bloom, Fred Hutchinson Cancer Research Center, Seattle,

video:

http://ncwebcasting.mediasite.com/mediasite/Play/2bf480aa266f494c854b39a1117179541d

Workshop 4C: Transmission and Infection Control
Meeting Room 2.60 (Level Two)
Chairs: Randy Albrecht, Icahn School of Medicine at Mount Sinai, Department of
Microbiology, New York, New York, United States of America
Sun-Woo Yoon, St. Jude Children’s Research Hospital, Memphis,
Tennessee, United States of America
Friday 28 Oral Presentations:
O-864 Biosafety and biosecurity in a biocontainment laboratory working with
highly pathogenic avian influenza (HPAI). Lisa Kercher
O-865 Utilizing endogenous microRNA to confer molecular biocontainment to
gain-of-function influenza viruses: towards risk mitigation. Randy Albrecht
O-866 Limited airborne transmission of influenza A/H7N9 virus between
ferrets. Eefje Schrauwen
O-867 Transmission bottlenecks in the ferret model differ between respiratory
droplet and contact transmission routes. Wendy Barclay
O-868 Efficacy of surgical face masks in reducing influenza virus dissemination
in human exhaled breath. Nancy Leung
O-869 Household transmission of influenza in Nicaragua. Aubree Gordon

video:

http://ncwebcasting.mediasite.com/mediasite/Play/2bf480aa266f494c854b39a1117179541d

Cox at ~1:00 influenza risk assessment tool (works without expert
probability estimates, avoids to estimate pandemic likelyhood, only impact)
Garcia-Sastre at
Kawaoka at 1:54 - 2:07
Lipsitch at 2:08-2:36
Simonsen at 2:36-2:40
Garcia-Sastre at 2:40-2:44
Russell at 2:44-2:53
Osterholm at 2:54-2:57
Kawaoka at 2:57-3:01
3:09 chances
...questions
3:17 end

**Shiloh** · November 6, 2014, 05:32 PM

Re: Man Made H5N1 - Super Version

Source: http://host.madison.com/wsj/news/loc...a7d9e4456.html

Yoshihiro Kawaoka's controversial flu research at UW-Madison on hold again
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2 hours ago ? By David Wahlberg | Wisconsin State Journal

Yoshihiro Kawaoka, a UW-Madison flu researcher, has halted his controversial flu research again after the White House requested that he and others doing certain experiments stop them during a review process.
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UW-Madison scientist Yoshihiro Kawaoka has once again halted controversial flu research, this time in response to a White House request that researchers stop such work during a federal review of the risks and benefits.

Kawaoka?s creation of an altered H5N1 flu virus in his lab led to a yearlong moratorium on such projects in 2012 after critics said the viruses could escape from the lab or be replicated by bioterrorists.

Kawaoka resumed the H5N1 work this May, after approval by federal and university officials.

But the Obama administration said Oct. 17 it would postpone federal funding for similar new studies and asked researchers to pause ongoing studies while the government develops a new policy.

The announcement covers ?gain-of-function,? or GOF, studies ? experiments that enhance the ability of a pathogen to cause disease ? involving influenza, SARS and MERS viruses.

Kawaoka said he complied with the request. ?In my laboratory, we paused all GOF experiments that might enhance pathogenicity or transmissibility,? he said in an email...

Announcement

Man Made H5N1 - Super Version

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