The efficacy of vaccination can be impaired considerably by even a mild coinfection; many and often conflicting reasons have been proposed for this phenomenon. Welsh and colleagues, in the Journal of Virology, use mice transgenic for a T cell antigen receptor specific for the male HY antigen or for virus peptide to determine how viral coinfection perturbs responses. Simultaneous triggering of HY- and virus-specific T cells results in robust responses by both populations; however, if the stimulation of HY-specific T cells is delayed by a few days, the responses to this antigen are lower. The possibility of activation-induced cell death or active killing by death receptors is ruled out; instead, the impairment coincides with the peak of virus-induced type I interferon (IFN-alpha or IFN-beta). Indeed, interferon stimulators such as poly(I:C) also impair the response of bystander HY-specific T cells much like viral infection, but not if the cells lack the receptor for type I interferon. These findings have important implications for the effective generation of vaccine and memory responses.
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机译：即使是轻度的合并感染，也会大大削弱疫苗接种的功效。已经针对该现象提出了许多且常常是相互矛盾的原因。 Welsh及其同事在《病毒学杂志》（Journal of Virology）中使用了对男性HY抗原或病毒肽具有特异性的T细胞抗原受体的转基因小鼠，以确定病毒共感染如何干扰反应。 HY和病毒特异性T细胞的同时触发导致两个种群的反应强烈。但是，如果将HY特异性T细胞的刺激延迟几天，则对该抗原的反应会降低。排除了激活诱导的细胞死亡或死亡受体主动杀死的可能性;相反，损伤与病毒诱导的I型干扰素（IFN-α或IFN-β）的峰值一致。确实，干扰素刺激物（例如poly（I：C））也像病毒感染一样削弱旁观者HY特异性T细胞的反应，但如果细胞缺乏I型干扰素受体则不会。这些发现对有效产生疫苗和记忆反应具有重要意义。
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