CD8 T-cell responses are directly affected by partial platelet depletion independent of the levels of circulating viral antigen. (A) Continuous platelet removal enhances LCMV Armstrong replication. Mice were treated with 1 dose (12 hours before infection), 2 doses (12 hours before and 2 days after infection), or 3 doses (12 hours before and 2 and 4 days after infection) of 40 μg of anti-GPIIb and infected with LCMV Armstrong intravenously. Serum viral titers were determined at day 8 after infection. (B) Effect of platelet removal on exhausted CD8 T cells. Mice were infected with the LCMV chronic strain clone-13, which in adult mice infects the WP, reaches higher titers in blood and peripheral tissues by day 4, and generates exhausted T-cell responses (C-D). Groups of mice were infected with the chronic LCMV strain clone-13 and treated with PBS or 40μg of anti-GPIIb 4, 6, and 8 days after infection. (C) Platelet depletion of LCMV clone-13 infected animals does not affect viral replication. Viral serum titers were determined after 15 days of infection. (D) LCMV-specific CD8⁺ T-cell responses during the course of a chronic infection are further affected by the absence of platelets. Two different CD8⁺, tetramer⁺ populations (D^bGP33 and D^bGP276) were quantified on day 15 LCMV clone-13 infected splenocytes. (C-D). Open bars, PBS-treated controls; black bars, anti-GPIIb–treated mice. Error bars represent SEM (*P < .05). One representative experiment of at least 2 is shown, with 6 animals per group.