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| -Short Attention Span Theater- |
| How to cure diseases before they have even evolved |
| 2009-08-12 |
| Very interesting, fairly long article from New Scientist. A taste: WILL swine flu virus turn nasty as the northern hemisphere winter gets under way? All previous pandemic flu strains started off mild before becoming deadlier, so health authorities are taking the threat seriously. They know that if 2009 H1N1 flu does become more lethal over the next few months, we will be nearly defenceless: there are already signs of resistance to Tamiflu, and any vaccines will be in very short supply. H1N1 flu is far from the only threat. A new pathogen could emerge at any time, as the SARS virus did in 2002, or a known virus such as that behind Lassa fever could become much better at passing from person to person and spread beyond Africa. Or a rogue scientist, or just a careless one, could release a deadly virus such as smallpox. We have been relatively lucky so far. The nature of SARS allowed it to be contained, while H1N1 flu remains mild for now. But our luck could run out tomorrow. "Mother Nature is among the worst terrorists," says Michael Goldblatt, who once led the biodefence programme for the Pentagon's research arm, DARPA, and now heads Functional Genetics, a biotech company in Gaithersburg, Maryland. How do you develop therapeutics for the unknown and unknowable, given that you won't have time to develop a vaccine for a new agent after it appears?" he asks. Goldblatt and a few other researchers think they have the answer. They are working on an entirely new class of antiviral drugs that should do something seemingly impossible: work against a wide range of existing viruses and also be effective against viruses that have not even evolved yet. What's more, it should be extremely difficult for any virus to become resistant to these drugs. This might sound too good to be true, but the first trials of these drugs are already producing encouraging early results. If just a few of them live up to their promise in full-scale human trials - no sure thing - they will be a medical breakthrough on a par with the discovery of penicillin. At last, doctors will be able to treat viral diseases as ably as they do bacterial ones. Back in the late 1990s, when Goldblatt was at DARPA, he began to wonder whether there was another strategy, one that exploits the key weakness of all viruses: their utter dependence on their hosts. By themselves, viruses are more helpless than newborn babies. They can replicate only by tricking their host cells into making more copies of them, a process that can involve hundreds of host proteins. What if, Goldblatt wondered, some host proteins are essential for viral replication but not for the survival of the host? If so, disabling these proteins should block viral replication without killing healthy cells. After moving to Functional Genetics, Goldblatt began putting his idea to the test. He and his colleagues disabled one gene at a time in human cells before exposing them to viruses such as flu. This fishing expedition worked beautifully: they identified more than 100 different human proteins that flu viruses need to replicate but which cells can survive without. Only four were previously known to be involved in viral replication. One especially promising target is TSG101, a protein involved in the transport of materials within cells that many viruses co-opt to break out of cells. Functional Genetics has developed a small-molecule drug that appears to block the interaction between viruses and TSG101. Dubbed FGI-104, the drug inhibits a wide range of viruses in cell culture, including hepatitis C and HIV, and has also been shown to protect mice against Ebola (American Journal of Translational Research, vol 1, p 87). |
| Posted by:Barbara Skolaut |
| #1 Very cool, Barbara -- I forwarded it Mr. Wife. Thank you! |
| Posted by: trailing wife 2009-08-12 23:57 |