| "CD4 molecules bind to one or more MHC molecules�molecules that might be called 'MHC CD4 compliment or ligand.'� | ||||
| Suppose those MHC elements were accidentally incorporated into a retrovirus, it seems possible that the retrovirus would then perform as HIV does. And the MHC elements, after all, are presumably independent cell surface molecules. The genes for making the MHC elements are in the human genome. And the bilipid layer of HIV has the same composition as the bilipid layer of those cells that have the MHC molecules. That�s because when HIV reproduces in a human cell, it snatches part of the cell�s bilipid layer to use as its own. So the appropriate MHC molecules should be right at home in a retrovirus bilipid layer. To reiterate, in a healthy person, CD4 molecules bind to one or more MHC molecules�molecules that might be called �MHC CD4 compliment or ligand.� I use that phrase because the three-dimensional conformation of two molecules that bind must be complimentary. But: CD4 molecules also bind to an HIV binding site. Is the same three-dimensional conformation presented by MHC CD4 ligand and the HIV site--or are they merely similar? And what about the two nucleotide sequences that generate those two conformations? Are they the same? . . . Or do two different nucleotide sequences generate two conformations that are similar enough to both bind to CD4? The human genome has been sequenced and so has HIV. Wouldn�t it be possible to locate and compare those two nucleotide sequences? I'm not a qualified specialist In any area of academic research. While it may seem to the reader that I rashly question those who know more than I, specialists generally operate with institutional or professional constraints. Such constraints may inhibit frankness. And sometimes it's instructive to put information obtained from different specialists together in an effort to focus on some specific social need. Thus I justify my role as a brutish generalist. In 2007 I found, with Google's help, that a CD4 ligand in a healthy person is interleukin-16. When HIV infection is present, CD4 ataches to HIV gp120. So my abstract question, above, became, "Are interleukin-16 and gp120 similar?" After a little more research, it appeared not, but that another MHC CD4 compliment or ligand region might be similar to gp120. With transposons and retrotrasposons moving about within the human genome and with the additional gene shuffling of meiosis, it seems to me that there might enough chaos involved in the aftermath of anal intercourse to allow the ad hoc assembly of HIV. For one thing, human sperm cells can penetrate cells other than a human ovum. A second point is that viruses are entities capable of self-assembly. Other non-viral cellular components such as membrane lipids, are also capable of self-assembly. Could, then, a virus assemble itself from components that might have become something other than a virus under different circumstances? One should keep in mind that if one viable virus could be produced "by accident," a multitude of progeny could well follow. A related question, under the scenerio we're trying to develop, is whether or not sperm cells could penetrate cells of the rectum following anal intercourse? It seems, from information provided by a reliable source, that they might. CONTINUE |
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