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Censoring influenza research: gagging scientists could put lives at risk

Scientists could reconstruct the work on the avian flu virus from clues, making suppression of future work counterproductive. AAP

Researchers working on a pathogenic strain of avian flu (H5N1) have agreed to pause their work for 60 days so international experts can discuss the safest ways to proceed. But it’s important to ensure that this voluntary moratorium doesn’t provide a platform for censorship of the research which has already faced calls for suppression of data from a US government agency.

Censorship of certain aspects of the research was proposed in the United States by the National Science Advisory Board for Biosecurity (NSABB), ostensibly in the interest of national security. The threat of such action led to urgent calls by scientists for globalization of the discussion. But arguments about the level of containment required for the work itself, and arguments about the suppression of publication have become confounded in the discussions of the research’s implications.

Wrong mutations?

It’s even been asserted that censorship won’t harm the health of our community because “limited benefit” will flow from this research – this is incorrect. Genetic changes made to the virus in this and earlier studies, which made changes based on those found in the 1918 “Spanish flu”, are based on naturally occurring mutations of the virus that have been implicated, by association (but not proven until recently), to cause severe illness in humans and animals.

It’s correct, as bioethicist Michael Selgelid pointed out in the Sydney Morning Herald that novel influenza viruses could conceivably evolve along unexpected paths, different from the ones tested in the work in question. But the identified mutations in this and related work are known (thanks to previously published work) to confer a selective advantage on the virus.

And these changes, or very similar ones, are those that will become common under selective pressure (just as specific drug resistance mutations in influenza A have become common because they confer a selective advantage).

Thanks to a substantial body of research already published in widely read scientific journals, all of us working in this field (and many of the scientifically literate public) already know that there are a handful of small but critical molecular changes in “high risk” regions in the virus. These changes have been repeatedly observed in naturally occurring influenza viruses and are not infrequent.


These mutations result in dramatic changes in virus behaviour. They’re implicated in virus attachment to carbohydrates in the lung and the spread of virus throughout the human body, outside the lungs.They can also tell us whether the virus is resistant to frontline anti-influenza drugs. They are, principally, mutations in the haemagglutinin gene segment, the polymerase and neuraminidase segments of the virus.

The research – of which some authors have been dismissive – is very important because it confirms the importance of these genetic changes for infectivity in a widely accepted and used animal model for human infection.

The molecular changes in “high risk” parts of the virus are also unquestionably valuable targets for vaccines and rationally designed drugs.

The work will pave the way for better community protection with new influenza inhibitors and vaccines targeting parts of the virus that have now been proven to be the causes of infectivity and fatality in mammals (similar methods, developed in Australia, have already proven their worth in the fight against Hendra virus).

If chemically identical or chemically similar changes are detected in the “high risk” regions of a new, seasonal influenza virus, diagnosticians and public health workers will immediately have the basis for quickly deciding whether special public health prevention measures are needed. This is preferable to using guesswork as has been used in the past, such as during the 2009 H1N1 outbreak in Mexico, which led to alarm and vaccine stockpiling.

Censoring too late

It’s obviously very important that work on living, highly pathogenic types of influenza virus be undertaken in high-level containment facilities. Access to living high pathogenicity virus should be strictly controlled (as is already the case in Australia, the United States and the European Union). But the suppression of publication of the genetic sequence information is a different issue and will not achieve security objectives.

At least in relation to “high risk” regions of the influenza virus – the cat has long been out of the bag amongst the broad community of infectious disease researchers. One of the recent research studies, targeted for censorship by NSABB was done by the group of Ron Fouchier of Erasmus Medical Center in Rotterdam, and has been submitted to the journal Science. Fouchier presented his results in September 2011 at an Influenza conference in Malta.


What’s more, partial publication of the work (as suggested by the NSABB) will not achieve the objective of suppression of methods. Sufficient information is already available to enable other research groups to independently make the same discovery (not many clues are needed for a competent scientist to figure out what has been done, even if not explicitly disclosed).

Notwithstanding the ability of scientists to reconstruct others’ work from clues, suppression of future work will be counterproductive, simply delaying access by our public health surveillance workers, diagnosticians and vaccine developers to specific information needed for community protection.

Suppression also presupposes (and, indeed, will ensure) that important additional discoveries will only be made within a preselected community of researchers (potentially, only military researchers).

Dual-use and other dilemmas

Bioethicists are rightly concerned about the dual-use dilemma (when research has the potential for both good and bad uses). But the line between single-use and dual-use technology is often fuzzy. Once governments start to draw definitional boundaries, potentially based on political, non-scientific considerations, those lines will inevitably move closer together. More and more papers could be suppressed or delayed.

Censorship could be misguidedly extended to block dissemination of vitally important information about mutations in Kunjin virus or Hendra virus that could affect the ability of those viruses to infect and kill horses and humans. Should we have suppressed the publication of the data showing that bats carry many virus diseases? Such knowledge could arguably be used for biological warfare.

There’s also the curly question of whether a single nation’s security advisors should dictate policy on what is publishable in the scientific community worldwide.

The bottom line is that, in the case of influenza virus research, tying the arms of our scientists behind their backs will put lives at stake and set a dangerous precedent. The ire of ethicists might be more appropriately directed at those political leaders who advocate censorship in order to restrict the use of knowledge for military or political purposes.

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