rCVB3.6 induces memory CD4⁺ T cells that expand in number and differentiate into secondary effectors following a challenge infection.

<p>Equal numbers (1×10⁴) of P14 and SMARTA cells from uninfected mice were combined and transferred into uninfected recipients. One to five days later, these mice were infected with rCVB3.3, rCVB3.6, or LCMV. Sixty to sixty-five days after the primary infection, the mice were challenged with LCMV (or left unchallenged), and P14 and SMARTA responses were analyzed on day 4 and 7 post challenge. Frequency of (A) P14 and (B) SMARTA cells as a percentage of CD8⁺ or CD4⁺ cells, respectively, in the blood of unchallenged and LCMV-challenged mice. Data are shown as the mean+SE of 6–16 mice per group, pooled from 4 independent experiments. (C) P14 and SMARTA responses in the spleens of these mice; the numbers in the dotplots indicate the percentage of transgenic cells among all mononuclear cells. (D) Changes in CD127 and CD62L expression on SMARTA cells following LCMV challenge of mice previously infected with rCVB3.6 (squares) or LCMV (circles). The percentage of SMARTA cells that were CD127^hi or CD62L^hi are shown as the mean ± SE of 2–4 mice per time point, pooled from 2 independent experiments; * p<0.05, ** p<0.005, *** p<0.001. The capacity of the transgenic and endogenous GP₆₁-specific CD4⁺ T cells to produce IFNγ and TNF (E), or IFNγ and IL-2 (F) was evaluated. Data are shown as the mean + SE of 2–4 mice per group, combined from 2 independent experiments.