Abstract
Recognition modes of individual T-cell receptors (TCR) are well studied, but how TCR repertoires are selected during acute through persistent human virus infections is less clear. Here, we show that persistent EBV-specific clonotypes account for only 9% of unique clonotypes but are highly expanded in acute infectious mononucleosis, and have distinct antigen-specific public features that drive selection into convalescence. The other 91% of highly diverse unique clonotypes disappear and are replaced in convalescence by equally diverse “de-novo” clonotypes. These broad fluctuating repertoires lend plasticity to antigen recognition and potentially protect against T-cell clonal loss and viral escape.
Footnotes
Funding: This study was supported by NIH grant AI-49320 (LKS+KL), AI-046629 (LKS+LJS), AI-109858 (LKS), AI038996 (LJS) and Center for Diabetes Research Core (DR32520), NIAID training grant T32-AI-007349–17 (LBW), the UMass Center for Clinical and Translational Science (UL1-TR001453), and a Nebraska Research Initiative grant to DG.