Intelligently designed avian flu?
First, as Luskin admits in the article, the answer to his titular questions is, "well, duh; of course it is." And alas, it doesn't get any better from there.
Allow me a moment to rant a bit here. It's painful for any expert in a field to read articles authored by those who are very clearly not trained in that area. I can't tell you how many times I've had to listen to local news media call Streptococcus or anthrax a "virus," for instance--something that probably doesn't bother normal people, but that makes me want to throw my TV out the window. (OK, or just write the station a nasty email). So, the little details that Luskin gets wrong are like nails on a chalkboard to me. For starters, there have not been 60 people "infected," as Luskin claims; there have been 60 recorded deaths, but we have no idea how many infections--certainly many times that number. As you'll see, this is probably the most minor of his blunders.
Second, Luskin claims:
Scientists suspect that this new "Avian Flu" strain of the flu virus arose because two flu viruses (probably one previously in humans, and another in birds), swapped genetic material in a process known as "reassortment."
Um, huh??? No, Casey, scientists don't claim this at all (and there's no link in his article where the statement by these mystery scientists is laid out)--and since this is central to your article, you really should have done some reading in this area. The thing scientists are concerned about is that this may happen--but it hasn't happened yet. The H5N1 viruses that are circulating are all bird, baby--no swapping has been detected. Kinda blows the whole "no new information--it's all horizontal transfer" thesis of the post, eh?
Luskin goes on to say:
So our fight to combat the Avian Flu is undoubtedly a fight against evolution. The question is, has there been a net increase in genetic information through this "evolution"? The Avian Flu is essentially the swapping of genes--but its genes probably came from other pre-existing viruses.
Nope; not as far as we can tell. We're not sure at this point why these particular strains of influenza are so nasty, and are able to infect so many different types of animals, but it's much more likely at this point that it's due to the accumulation of minor point mutations (antigenic drift) rather than the reassortment--or antigenic shift--that he's referring to.
Keeping these blunders in mind, let's look at Luskin's next point:
One new twist on the Avian Flu is that it can infect organs other than the lungs and cause damage to greater parts of our bodies. This more widespread attack has caused some fatalities. The fact that the Avian Flu can activate this protein in other places probably has something to do with its new configuration of genes. But we're really not dealing with anything new.
Since no significant "new configuration of genes" has occurred, Mr. Luskin, wouldn't this ability to infect a wider range of organs--likely due to subtle changes in the influenza virus proteins--now be a "gain of information?" If not, what then, pray tell, would constitute such a gain?
After a discussion of mutation limits, he continues...
Viruses are masters at taking what already exists and swapping it around to dodge our immune system. And that's what has happened here. It's still a virus, and there's probably nothing "new" in terms of new genes. This does not show that evolution can create new genetic information.
But as I pointed out above, that's not what's happened here; and indeed, that's not what happens in many pathogen species that show high levels of antigenic diversity. For example, let's take a look at the bacterium once thought to be the cause of influenza, Haemophilus influenzae:
To facilitate evasion of the immune response generated by the human host, H. influenzae has evolved several molecular mechanisms by which to alter the antigens on its surface.
Point mutations. Antigenic diversity of proteins occurs most simply, and perhaps most commonly, by spontaneous point mutations in the genes encoding protein antigens, such that the physical topography of the molecule is altered and antibodies directed against the original antigen do not recognize the altered one.
Would this be "new information?" Why or why not?
Gene amplification. The Hib capsular genes have been studied in detail and are located in a chromosomal region characterized by two tandem 18-kilobase repeats. The quantity of type b capsular material expressed is proportional to the number of tandem repeats present in an isolate, with a maximum of five repeats identified. Nonencapsulated variants arise at relatively high frequency (0.1 to 0.3%) and are characterized by deletion of one of the tandem repeats such that the remaining copy lacks bexA, a gene required for polysaccharide export.
Does this constitute "new information?" Why or why not?
Phase variation. Phase variation is a method by which organisms alter the expression of surface molecules in a reversible fashion. Phase variants arise from the background population of bacteria at relatively high frequencies and may be selected during changing environmental conditions. Two H. influenzae surface molecules, pili and LOS, undergo phase variation, and the genetic mechanisms responsible for this variation have been, at least partially, elucidated. The factors that stimulate, or facilitate, phase variation of these antigens have not been defined, although the presence of a specific antibody may result in enhanced survival of either organisms expressing an alternative antigenic form of phase variable antigens, as in LOS, or organisms not expressing the antigen at all, as in pili.
Horizontal gene transfer and recombination. H. influenzae, like other human mucosa commensals such as Neisseria gonorrhoeae and S. pneumoniae, is naturally transformable in that it possesses specific mechanisms for importing DNA from the environment.
I guess we already know the answer to this one.
In her review, Dr. Gilsdorf also notes that:
Another potential mechanism for antigenic variation in bacteria is posttranslational modification, such as glycosylation, phosphorylation, sulfation, or sialylation, of surface proteins.
As Andrea Bottaro's post on prions pointedly reminds us, the genetics sure as heck ain't the end of the game. What about this type of regulation of antigenic variation? And while the mechanisms of antigenic variation listed above are fairly common in a variety of bacterial species, there are certainly others not listed above to take into consideration as well. A bit more complicated than Luskin makes it out to be, methinks.
Ah well, back to the nails on the chalkboard:
But there's good news. Scientists are working on creating antibodies.
Funny, I thought we were working on creating vaccines. But hey, what do I know?
And then, just when you think it can't possibly get any worse, the final coup de grace:
In conclusion, viruses are constantly trying to out-evolve your immune system. That's how they survive. All they can do is mutate certain non-essential portions of their DNA within a mutation limit, and try to acquire other pre-existing genes to create combinations your antibodies haven't seen before. But in the end they're still always viruses.
No. He did not write that, did he?? "But they're still viruses!" has to be one of the most moronic phrases in the anti-evolution bag of tricks. I know I shouldn't expect it, but for whatever reason, I tend to hold the DI and their mouthpieces up to a slightly higher level than the other creationists. I have my mental ladder, with Kent Hovind down at the bottom, Ken Ham et al. up a rung, 'cause at least even they think Hovind's a nut, and then the DI up a rung above that, since at least they're not trying to force everyone to believe the world is 6000 years old. But then Luskin has to go and obliterate what little, tiny, minute scintilla of props that I gave to the DI for being less crazy than the other creationists. At least he did encourage getting flu shots--I suppose I should take some comfort in that. And also, since their website is devoted to correcting inaccuracies in the media...
The misreporting of the evolution issue is one key reason for this new site. The newsmedia in the U.S. seem to have rediscovered the evolution controversy recently. Unfortunately, much of the news coverage has been sloppy, inaccurate, and in several cases, overtly biased.
...I'm sure someone will rush right in and correct Luskin's sloppy, inaccurate, and in some cases, overtly biased piece, so that the evolutionnews site lives up to the lofty standards they expect of others.