Coxsackievirus B3 almost completely inhibits antigen presentation via the MHC class I pathway, evading CD8+ T cell immunity, while inducing functional CD4+ T cell responses via the MHC class II pathway.
Coxsackievirus B3 selectively evades CD8+ T cell immunity by inhibiting MHC class I antigen presentation, while leaving MHC class II presentation and CD4+ T cell responses intact.
Many viruses encode proteins whose major function is to evade or disable the host T cell response. Nevertheless, most viruses are readily detected by host T cells, and induce relatively strong T cell responses. Herein, we employ transgenic CD4(+) and CD8(+) T cells as sensors to evaluate in vitro and in vivo antigen presentation by coxsackievirus B3 (CVB3), and we show that this virus almost completely inhibits antigen presentation via the MHC class I pathway, thereby evading CD8(+) T cell immunity. In contrast, the presentation of CVB3-encoded MHC class II epitopes is relatively unencumbered, and CVB3 induces in vivo CD4(+) T cell responses that are, by several criteria, phenotypically normal. The cells display an effector phenotype and mature into multi-functional CVB3-specific memory CD4(+) T cells that expand dramatically following challenge infection and rapidly differentiate into secondary effector cells capable of secreting multiple cytokines. Our findings have implications for the efficiency of antigen cross-presentation during coxsackievirus infection.
Kemball et al. (Thu,) conducted a other in Coxsackievirus B3 infection. Coxsackievirus B3 (CVB3) infection vs. LCMV infection or uninfected controls was evaluated on Antigen presentation via MHC class I and II pathways and subsequent T cell activation. Coxsackievirus B3 almost completely inhibits antigen presentation via the MHC class I pathway, evading CD8+ T cell immunity, while inducing functional CD4+ T cell responses via the MHC class II pathway.
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