... Except how to read.
Towards the end of The Great UD Adventure, Sally decided he knew more about HIV and the HIV research world than me. Granted, lots of people do know a hellovalot more about HIV research than me.
But Sal is not one of those people.
So like I did before, lets use Creationist Behavior as a learning opportunity!
I’m having problems accepting that viropoin capability was novel after emergence in humans in light of this paper:
Now, dont laugh at him. Reading is really hard for some people. Maybe he didnt notice the title of the paper he cited:
To date, no studies have been performed to assess the role of this domain in virus pathogenesis in a macaque model of disease. Using a pathogenic molecular clone of simian human immunodeficiency virus (SHIVKU-1bMC33), we have generated a novel virus in which the transmembrane domain of the Vpu protein was scrambled but maintained hydrophobic in nature (SHIVTM), which presumably would disrupt any ion channel TM properties of this protein
Thus, these results show for the first time that the TM domain of Vpu contributes to the pathogenicity of SHIVKU-1bMC33 in pig-tailed macaques.
This paper would appear to weaken the claim that even if “Viroporin capabilities have not been found with SIVcpz Vpu”, that they emerged brand spanking new in humans.
Thus, this would appear not to be an appropriate counter example to Behe’s claims. The fact that one may not see a function in one strain does not imply that it emerged brand new in another strain. It is entirely possible this was a loss of fucntion, and with respect to the issue of this viroporin capability, it was a loss of function (if at all).
Speaking of which, were there even studies done on SIVcpz regarding scrambling of the TM domain? Can’t very well find them if one doesn’t even look for them.
Scrambling of the amino acids within the transmembrane domain of Vpu results in a simian-human immunodeficiency virus (SHIVTM) that is less pathogenic for pig-tailed macaques.
Thats less pathogenic, folks. Screwing with Vpu makes SHIVs less pathogenic.Maybe Sal doesnt know what a SHIV is. Hmm... That cant be possible, because the authors of that cited paper define their SHIV right in the intro:
The simian-human immunodeficiency virus (SHIV) is a chimeric virus that contains the tat, rev, vpu, and env genes in a genetic background of SIVmac239.The tat, rev, VPU, and env genes are from HIV-1. The remaining proteins come from SIVmac. Creating these chimeras is one way we can study AIDS in non-human primates. For instance, pig-tailed macaques cannot be infected with HIV-1, but if you exchange a few HIV genes with SIVmac genes, you can infect them and study AIDS at an organismal level!
And lo and behold, thats exactly what the authors did.
Our laboratory has been using a pathogenic simian-human immunodeficiency virus (SHIV)/macaque model to examine the role of Vpu in disease. Using the pathogenic molecular clone SHIVKU1bMC33, we previously showed that an intact Vpu contributed to the CD4+ T cell loss that occurs during infection with the pathogenic SHIV and that disease in macaques only occurred if compensating amino acid substitutions occurred in the Env and Nef proteins. In order to study the role the TM plays in vivo to enhance pathogenesis, we constructed a mutant SHIV virus (SHIVTM) in which the TM domain of the Vpu protein was scrambled but kept hydrophobic as previously described. In this study, we have analyzed the in vitro replication of this virus and its ability to cause CD4+ T cell loss and disease in macaques. Our results indicate that SHIVTM was not as pathogenic to pig–tailed macaques as the parental SHIVKU1bMC33, indicating that the TM domain contributes in part to the rapid CD4+ T cell loss and disease onset caused by SHIVKU1bMC33.If you screw up the transmembrane region of HIV-1 Vpu, you get a less pathogenic virus that cant kill CD4 cells as efficiently. Thats what I said. So in addition to no experimental evidence for viroporin formation (see my essay references), this group found no genetic or biochemical reason to expect viroporin capabilities in SIVcpz. Thats also what I said.
You could have read my essay 100 times in the amount of time it took you to find that paper, Sal. Read. Read slowly. And then think reaaaal hard about whether you want to ask an HIV researcher a question, or whether you want to tell that HIV researcher you know more about her specialty than her. Save you some embarrassment in the future.