• FluTrackers.com Inc. does not provide medical advice. Information on this web site is collected from various internet resources, and the FluTrackers board of directors makes no warranty to the safety, efficacy, correctness or completeness of the information posted on this site by any author or poster. The information collated here is for instructional and/or discussion purposes only and is NOT intended to diagnose or treat any disease, illness, or other medical condition. Every individual reader or poster should seek advice from their personal physician/healthcare practitioner before considering or using any interventions that are discussed on this website. By continuing to access this website you agree to consult your personal physican before using any interventions posted on this website, and you agree to hold harmless FluTrackers.com Inc., the board of directors, the members, and all authors and posters for any effects from use of any medication, supplement, vitamin or other substance, device, intervention, etc. mentioned in posts on this website, or other internet venues referenced in posts on this website.
  • We are not asking for any donations. Do not donate to any entity who says they are raising funds for us.

Biologists risk becoming accidental terrorists-NewScientist

Mingus

Well-known member
http://www.newscientist.com/channel/opinion/mg19025555.700.html;jsessionid=NBADKCECMFKF


Biologists risk becoming accidental terrorists


* 10 June 2006
* From New Scientist Print Edition. Subscribe and get 4 free issues.
* Peter Aldhous

“In just a few years, designer bioweapons could be within reach of a rogue state”



FOR anyone who doubts that well-intentioned research can sometimes have potentially deadly consequences, Ron Jackson has a cautionary tale. Working for the wildlife division of Australia's national research agency, he set out to make a contraceptive vaccine to control plagues of mice. What he ended up with was a deadly mousepox virus that resists vaccination - and a recipe for doing the same for smallpox.

This story, revealed by New Scientist more than five years ago (13 January 2001, p 4), caught everyone off guard. Then came the 9/11 terrorist attacks and the anthrax letters. Bioterrorism was propelled to the top of official worry lists in the US, and it was clear that legitimate research could produce pathogens much nastier than anthrax.

Despite these fears, it seems to me from my reporting on these issues that many biologists remain ignorant of the "dual-use" dilemma - that biological advances can provide a bioweapons cookbook. Researchers trying to improve human health by, for example, altering specific immune responses rarely consider that the same technologies could be converted into horrifying weapons.

Thankfully, Al-Qaida is not thought to have the expertise to create designer bioweapons. In a few years, however, such capabilities may well be within reach of a rogue state willing to invest large sums in clandestine research. This does not mean that all data that could be turned to destructive ends should be declared a military secret - although a small proportion might need to be classified. It does mean that biologists should pay more attention to the sinister potential of their work and avoid lines of enquiry that pose more dangers than they promise benefits.

Scientific societies should be raising awareness of these issues among their members, and the American Society for Microbiology (ASM) points the way. Its website hosts a wealth of resources on bioterrorism and biosecurity. Other societies are still lagging behind. The American Association of Immunologists has yet to adopt relevant policies, even though manipulation of the immune system is central to this debate. Jackson's deadly mousepox owed its pathogenicity to an unexpected effect of IL-4, an immune-signalling molecule. He engineered a strain of mousepox to produce proteins carried by mouse eggs, and reasoned that adding the gene for IL-4 would stimulate antibodies against these proteins, sterilising the mice. Instead, it shut down the cellular arm of the immune system, needed to fight viral infection.

Journals also have a role to play. Many now scrutinise the papers they receive to avoid publishing information that poses serious security concerns, though few papers merit censorship. Much more useful is the promotion of debate around dual-use research. This has happened in obvious cases such as the recreation of the virus that caused the 1918 flu pandemic, but other papers with bioweapons potential continue to appear without comment.

Take a paper on a new vector for gene therapy, published in February by Nature Biotechnology (vol 24, p 198). Researchers at the University of California, Berkeley, used "gene shuffling" technology, a form of accelerated evolution, to create harmless viruses that are able to evade "neutralising" antibodies. It is a valuable project, because these antibodies can wipe out viral vectors before they deliver their therapeutic genes. The danger is that the same approach could help deadly viruses slip under the immune system's radar. Lead researcher David Schaffer told me that he would never attempt anything similar with a human pathogen, but neither his paper, nor the commentary on the work published with it, mentioned the dual-use potential.
“In just a few years, designer bioweapons could be within reach of a rogue state”

Even when researchers address the implications of their work for biowarfare, some of their ideas on tackling the problem are naive. At the heart of synthetic biology lies the ability to build large sequences of DNA, and even entire viruses, from scratch. It may be possible to obtain DNA to build a bioweapon from companies that synthesise genes to order (New Scientist, 12 November 2005, p 8). At the Synthetic Biology 2.0 meeting in Berkeley last month, researchers pledged to develop better methods of identifying suspect orders, yet in the online debate that preceded it one graduate student suggested placing "malicious orders" to test the effectiveness of companies' screening procedures. Although some sort of verification may be useful, posing as a terrorist would be seriously misguided, and depending on the sequences requested could breach US anti-terror law.

This incident points to perhaps the most urgent need: better education of graduate students. Few universities offer classes in biosecurity, and given the dearth of experts in the field, they have some excuse. But not for much longer: within the next month, the Federation of American Scientists will be releasing a biosecurity curriculum, complete with dual-use case studies, including an interview with Jackson. It should be a required option for anyone planning a career in biomedical research.

From issue 2555 of New Scientist magazine, 10 June 2006, page 24
 
Re: Biologists risk becoming accidental terrorists-NewScientist

Jackson's deadly mousepox owed its pathogenicity to an unexpected effect of IL-4, an immune-signalling molecule. He engineered a strain of mousepox to produce proteins carried by mouse eggs, and reasoned that adding the gene for IL-4 would stimulate antibodies against these proteins, sterilising the mice. Instead, it shut down the cellular arm of the immune system, needed to fight viral infection.

IL-4 is a cytokine !

It is interesting to note that they think that add a cytokine gene in a virus would stimulate the immune system but instead, it disable it...

Very dangerous, never do something like this again and risk to loose this thing in the wild.
 
Re: Biologists risk becoming accidental terrorists-NewScientist

J. Virol., Aug 1996, 5230-5235, Vol 70, No. 8
Copyright © 1996, American Society for Microbiology


Interleukin-4 causes delayed virus clearance in influenza virus- infected mice
TM Moran, H Isobe, A Fernandez-Sesma and JL Schulman
Department of Microbiology, Mount Sinai School of Medicine, New York 10029, USA.

Two different subsets of T cells, Th1 and Th2 cells, have been demonstrated to secrete different profiles of cytokines and to influence various infections in different ways. Whereas cytokines secreted by Th1 cells, particularly gamma interferon, promote the generation of cell-mediated immunity, Th2 cells and their cytokines (interleukin-4 [IL-4], IL-5, IL-10, and IL-13) have been shown to function in recovery from parasitic infections and in antibody responses. In this study, we analyzed the effects of the dominant Th2 cytokine, IL-4, on immunity to virus infection. We assessed the effects of IL-4 on both secondary immune responses by an adoptive transfer assay and primary immune responses by in vivo treatment of influenza virus-infected mice with IL-4. The results demonstrated that IL-4 can function to inhibit antiviral immunity at both stages. We found that IL- 4 treatment of sensitized cells during secondary stimulation in vitro had little effect on their ability to lyse virus-infected target cells in a 51Cr release assay. Nevertheless, the clearance of influenza A/PR/8/34 (H1N1) virus from the lungs of infected BALB/c mice was significantly delayed after the transfer of virus-specific T cells secondarily stimulated in the presence of IL-4 in comparison to virus clearance in recipients of cells stimulated in the absence of IL-4. In contrast to the adoptive transfer results, the treatment of PR8 virus- infected mice with IL-4 during primary infection greatly suppressed the generation of cytotoxic T-cell precursors, as assessed by secondary stimulation in vitro. In addition, culture supernatants of secondarily stimulated spleen cells from IL-4-treated mice contained significantly less gamma interferon and more IL-4 than did spleen cells from controls. More importantly, the treatment of mice with IL-4 resulted in an extremely significant delay in virus clearance. Thus, IL-4 can inhibit both primary and secondary antiviral immune responses.
http://jvi.asm.org/cgi/content/abstract/70/8/5230
 
Re: Biologists risk becoming accidental terrorists-NewScientist

It appear that we cannot conclude simplistic conclusion.

In some situation one kind of cytokine does a beneficial effect.
In other situation this same kind of cytokine does a negative effect.

All thoses mediators of the immunitary response seem to act in a very fragile equilibrium and any atemps to modify this equilibrium give us unexpected results.

I don't think this process is well understood by the science of today's time.
There is much more work to do.
 
Back
Top