Alloantigen-stimulated anti-HIV activity occurs prior to reverse transcription (panels A, B, and C) and is generated in the absence of an intact CD28/B7 costimulatory pathway (panels D, E, and F).

PHA blasts were infected with HIV-1_BZ167 (172 TCID₅₀/10⁵ cells) and cultured in the absence (control) or presence of an HIV-suppressive supernatant derived from an alloantigen-stimulated cell line (Allo).3 Levels of LTR-gag (A) and LTR U3/R HIV-1 reverse transcripts (B) in HIV-1_BZ167-infected PHA blasts were determined by quantitative, real-time DNA PCR.7,8 Results in panels A and B represent means (number of copies/50 000 ± 10 000 cells) ± standard deviation of 2 independent experiments. HIV-1 p24 antigen production by HIV-1_BZ167-infected PHA blasts (C) was determined by ELISA. Alloantigen-stimulated supernatants from cultures performed in the absence (−) or presence of CTLA4Ig fusion protein (5 μg/mL) added at the beginning of 7-day cultures7 were assayed for effect on HIV-1_BZ167 replication in T-cell blasts (D) and IL-2 production (E) measured by ELISA. Alloantigen-specific proliferation (F) was measured 7 days after primary stimulation. Results are expressed as mean ± SEM of 3 (D), 5 (E), and 6 (F) independent experiments.