Dear Laszlo,
Your comments are well taken, but I beg to differ with your inference that direct infection is of little consequence to the function of T-cells. I think that the apoptosis work is indeed very interesting, but it is quite a jump to imply that cells other than those infected should be comparatively worse off than the targets (cd3+ lymphocytes, to be safe). While other cells MAY be involved, I believe it would be a mistake to assume that the direct targets don't mind so much to have a bit of foreign DNA in their genomes.
The fact is that retroviral integration into a host impairs immune funtion drastically. It just takes time to do so in the case of HIV. Please note the case of HTLV-1 (HIV-1=HTLV-3), a virus very similar to HIV which shares the same host cells. It has been shown by Yoshida et al, and others that while
HTLV is not active in most infected cells (that is, little or no message production), the CD8+ and CD4+ cells lose their ability to repond to antigen.
So, even if they aren't actually lysed, the cells are very much affected.
I agree that there must be some precursers in the periphery or somewhere.... Where else could memory CTLs or even new CTLs come from?
Christopher Savoie
Department of Genetics
Medical Institute of Bioregulation
Kyushu University
