NKG2A+ NK Cell Cytotoxicity of Epstein-Barr Virus Infected B Cells is Mediated Through the NKG2D and NKp30 Activating Receptors
Epstein–Barr virus (EBV) is a ubiquitous gamma-herpesvirus that persists as a chronic, asymptomatic infection in over 90% of the adult human population. EBV infections are mainly asymptomatic and subside due to a vigorous host T cell response with the virus transitioning to latency in a subset of memory B cells. Failure to control latent EBV infection can result in a variety of EBV-associated malignancies, including lymphoproliferative diseases in immunocompromised people. Studies in both experimental models and humans suggest that NK cells are critical in the host defense against EBV. In this study we utulized scRNA-seq to better understand the phenotype of NK cells that respond to EBV-infected B cells. We generated a panel of EBV+ lymphoblastoid cell lines (EBV+ LCL) and performed coculture experiments with primary NK cells and their autologous EBV+ LCL  using 10x Genomics scRNA-seq. Subsequent analyses following alignment and data processing were completed in Python. Overall design: Following coculture with an autologous EBV+ LCL, cells were sorted for CD107a+ (responsive) and CD107a- (nonresponsive) NK cells using scRNA-seq.