Galpin/DA/N2 UIBenv 
3.4.1 Regarding human PBMC-derived CTL, the following statements can be 
made: 
(1) HIV-IT (V) can transduce human lymphoblastoid cell lines derived from HIV 
infected individuals and these transduced cells can present HIV-1 IIIB antigen 
for recognition in each of the three related in vitro CTL assays described above. 
(2) Measurement of human CTL responses with these assays is feasible, and one or 
more is likely to have utility in monitoring human clinical responses to 
HIV-IT (V). 
(3) All HIV-infected patients studied to date have measurable endogenous levels of 
CTL activity which have no obvious correlation with their CD4 counts. 
(4) All HIV-infected patients with CD4 counts of 260 and above studied to date 
exhibit CTL activation in vitro. 
(5) In vitro stimulation of CTL responses with HIV-IT (V)-transduced autologous 
cells presenting HIV-1 IIIB env epitopes is effective. This appears to represent a 
recognition of CTL elicited in vivo by unknown HIV-1 strains infecting these 
patients. This suggests by analogy that the CTL crossreactivity between HIV-1 
strains seen in the mouse CTL/human target system (Section 3. 1.1. 6) applies also 
to the CTL existing within HIV-infected patients. 
3.4.2 Conclusion 
Preclinical evaluation of the HIV-1 IIIBenv/rev retroviral vector (N2 IIIBenv) 
has demonstrated it to be free of adventitious agents, to be biologically active both in 
vivo in eliciting CTL both in mice and in primate models, and in vitro in generating 
both stimulator and target cells for use in assays of CTL from HIV- 1 -infected patients. 
Evidence obtained from the human CTL assay using stimulated patient PBMC as 
effectors demonstrates provocative evidence for cross-activation of human CTL by 
HIV-IT (V). This in vitro demonstration that HIV-IT (V) can reactivate human 
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