Early control of the virus is affected by partial platelet depletion independent of type I IFN production. Mice were treated with 3 doses (12 hours before and 2 and 4 days after infection), 2 doses (2 and 4 days after infection), or 1 dose (4 days after infection) of 40 μg of anti-GPIIb and infected with LCMV Armstrong intravenously. (A-B). (A) Platelet presence in the first 2 days of infection is needed to control the infection. Eight days after infection viral titers in serum were determined. (B) Functional exhaustion of LCMV specific CD8 T cells is restored if platelets are present in the first 2 days of infection. Intracellular IFNγ and TNFα cytokine production by day 8 splenocytes after in vitro stimulation (numbers in flow plots indicate percentage of cells inside gates). Mice were treated with 40 μg of anti-GPIIb and infected intravenously 12 hours later with LCMV Armstrong (C-D). (C) Equivalent LCMV replication in spleen and liver but higher titers in lungs 48 hours after infection in the absence of platelets. Viral titers in spleen, liver, and lung tissue homogenates. 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. (D) LCMV-induced antiviral IFN-α/β levels. Mice were bled at 6, 12, 24, and 48 hours after infection and IFN-α/β bioactivity was determined in serum (n = 4-6 animals, in 2 independent experiments; error bars represent SEM).