Drugs, Vaccines, Surveillance for Influenza All Get Boosts

Tag : avian influenza

The Virtues of Sharing
The bad news is that influenza kills between 250,000 and 500,000people annually. The worse news is that that's just the seasonalstrains.
At irregular intervals, new strains that cause pandemics arise. Thefatality count of pandemics depends on how nasty the pandemic flustrain is. But the avian flu strain H5N1 that many see as the topcontender for the next pandemic could lead to fatalities in thetens of millions.
The July 10, 2008, issue of Nature combines policy calls for improvements in the fight againstinfluenza with research news showing where new drugs for that fightmight come from.
A commentary by officials from the Bill and Melinda GatesFoundation, the Institute Pasteur and the Wellcome Trust urges thedevelopment of a vaccine stockpile - including the possibility ofusing pre-pandemic strains that would not likely produce thestrongest possible immune response to the final pandemic strain,but could be prepared in advance.
A paper in the August, 2008, Journal of General Virology might help with the selection of such pre-pandemic strains:researchers try to take some of the guesswork out of which flustrains are most likely to be pandemic culprits, by investigatingthe mutations that H5N1 undergoes during the course of aninfection. The authors, who are from Mahidol University inThailand, report that some mutations occur more frequently thanothers, suggesting they represent a form of successful adaptationto human hosts. The authors suggest their method could be used toimprove surveillance of potential pandemic strains.
The Nature commentary also highlights the need for openness in sharingscientific information ranging from flu strain to surveillancedata. A separate commentary in Nature , this one specifically addressing last year's more-or-lessineffective seasonal flu vaccine, echoes the need for sharing data- and is blunt about the dire consequences that can result from alack of openness in the strain selection process. The 2007-2008vaccine was only about 40 percent effective at preventing influenzacases, and commentary author Steven Salzberg from the University ofMaryland lays the blame for the failure squarely at the doorstep ofthe vaccine design system's secretiveness.
The failure "could have been predicted, if not prevented, through amore open system of vaccine design, a stronger culture of sharingin the influenza research community and a serious commitment to newtechnologies for production" he writes. "The habits of the vaccinecommunity must change for the sake of public health."
Salzberg points out in his commentary that currently, the meetingthat determines which flu strains will be used in a seasonalvaccine is invitation-only - and that not everyone who has ameaningful contribution to make is invited. Even after the meeting,the data that the WHO uses to arrive at its recommendation is notmade public, making it impossible for external scientists toevaluate it, let alone suggest improvements. This culture ofsecrecy, he argues, is also apparent in the sharing of flu strainsequence data - or the lack thereof.
Salzberg points out that even the WHO centers oftentimes either donot share their sequence data, or "share" it in a subscribers-onlydatabase rather than a truly public one such as that of the GlobalInitiative on Sharing Avian Influenza Data.
Scientists reported this week on using the fruit fly drosophila as a screening tool to identify potential cellular proteins thatcould be targeted to fight the flu. Asked what the advantage ofusing an engineered virus is over going directly into human cellculture, senior author Yoshihiro Kawaoka - who also noted that"engineering the virus is not difficult" and his group, in fact,has a decade's worth of experience with it by now - told BioWorld Today that "when we started our project, the siRNA library for humancells was not complete." Only about a third of human genes could beknocked down with siRNA at the time, as opposed to roughly 90percent of fly genes.
The researchers engineered the flu virus, which normally does notinfect fly cells, with new surface proteins that enabled it toenter, and then screened a siRNA library of about 13,000 sequencesto knock down cellular proteins in the hopes of finding novel drugtargets that can stunt viral growth by working on host proteinsrather than on the virus itself. The researchers identified over ahundred such genes, including three that are known to play keyroles in enabling viral replication in human cells. The researchersthen confirmed the three genes in human cell lines, using bothseasonal influenza virus and a strain of H5N1 isolated from apatient in 2005.


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