Sunday, August 12, 2007

Send in the pawns! Part Deux!

A well meaning Creationist poster at Pandas Thumb bravely attempted to defend Behe (once again, Behe prefers to let other people defend his incompetency). He cited a paper that proclaims:

Both Vpr- and Vpu-induced apoptosis involve the activation of the caspase pathway (references 48 and 49, and this study). Although the precise mechanism for Vpr-induced apoptosis is still unclear, recent observations suggest that it might be caused by a Vpr-induced permeabilization of mitochondrial membranes resulting in the release of apoptogenic proteins such as cytochrome c or apoptosis inducing factor and the subsequent activation of caspase (50). While it was suggested that Vpu itself might have poreforming properties (51, 52) making a mechanism for induction of apoptosis similar to that of Vpr conceivable, our data suggest that Vpu instead functions by inhibiting the NF-{kappa}B–dependent expression of antiapoptotic genes.
There is a lot wrong with this, and I want to make it clear I do not blame Collin for not understanding why his quote does not save Behe. Behe hasnt even attempted to defend himself-- kudos to Collin for trying. We can at least use Collins attempt as a learning opportunity.

The referenced paper addresses one question and one question only: Does Vpu effect apoptosis?

Thats it.

Not whether Vpu forms ion channels, but if Vpu sets off some kind of cell suicide pathway. Viroporins are more of a side comment in the discussion section, not the foundation of the papers hypothesis.

This paper does not support Behe-- It makes things worse. Vpu might have yet another trick up its sleeve. It might interact with a cell death pathway.

Or it might not:
It has also been shown that HIV-1 particle adsorption, even of defective particles, can induce efficient activation-dependent apoptosis in bystander CD4+ and CD8+ T cells. In addition, secreted HIV-1-encoded proteins, such as Tat, Nef, or Vpr, and apoptosis-inducing factors released from HIV-1-infected cells, such as Fas ligand, tumor necrosis factor alpha, or tumor necrosis factor-related apoptosis-inducing ligand, have all been shown to trigger apoptosis in uninfected bystander cells. On the contrary, several hypotheses derived from in vitro studies have investigated possible mechanisms for the direct killing of infected cells, as follows. Apoptosis induction by recombinantly expressed Env, Tat, Nef, Vpr, and Vpu has been demonstrated. However, much of the evidence on mediators of HIV-1-induced cell death is contradictory. For example, Tat has been associated with apoptosis induction in some studies, while other studies have shown its protective role against apoptosis. The wide variability of these findings may be due, at least in part, to the fact that most of these studies have examined the effects of large amounts of recombinant HIV-1 proteins artificially expressed in various kinds of cell lines.
Translation: Vpu might kill infected cells directly, but the studies that have demonstrated that werent exactly carried out in a realistic manner. Think of the artificial sweetener studies-- If you give a mouse 50 pounds of fake sugar to eat, hes gonna get a tumor. Pump a cell full of Vpu, the cell is going to die. This paper cites Collins paper directly, as one of those 'not-exactly-realistic' studies.

But Klaus Strebel was the first author on one of the papers reporting the discovery of Vpu-- Im going to listen to him when he talks about Vpu. We will just have to see where research leads Vpu.

But this doesnt effect the fact that Vpu whomps Behes claims about HIV in 'Edge of Evolution.'

So good try, Collin. Im still waiting for Behe.

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