The reader may want to take a look by clicking this line.
On this site I found the statement that “diversity [of HIV] seen in patients is the result of large numbers of virions present in the patient and the high rate of replication (Coffin 1995).” But that doesn’t explain why HIV has a much higher RATE of variability— variability, that is, PER a given number of viruses--than other retroviruses. Variability produced by meiosis could provide an explanation. The scientist who was just quoted was Dr. John M. Coffin of Tufts School of Medicine. I talked to him on the phone to give him a chance to comment, but he hadn't done so as of the time of this revision of my material.
Another factor contributing to variability, possibly, is HIV recombination within cells. But why should HIV have a unique ability to do that which other retroviruses lack? I have some other questions about that which I won't try to go into here.
I did speak by phone with Dr. Theodore Jardetsky of Northwestern. He didn’t agree with my ideas as expressed here and pointed out that the retroviruses in the human genome aren’t HIV.
That’s true, but, as mentioned previously, when HIV infects humans, the virus attaches to a molecule known as the “CD4 molecule.” The virus does that before entering those cells that have that CD4 molecule. Once inside a CD4 cell, a virus may reproduce. But in normal healthy functioning of the immune system, according to Dr. Jardetsky, the CD4 molecule functions by attaching to elements of the major histocompatability complex (MHC).
CONTINUE