Time-resolved transcriptomes reveal diverse B cell fate trajectories in the early response to Epstein-Barr virus infection.
Epstein-Barr virus infection of B lymphocytes elicits diverse host responses via well-adapted transcriptional control dynamics. Consequently, this host-pathogen interaction provides a powerful system to explore fundamental processes leading to consensus fate decisions. Here, we use single-cell transcriptomics to construct a genome-wide multistate model of B cell fates upon EBV infection. Additional single-cell data from human tonsils reveal correspondence of model states to analogous in vivo phenotypes within secondary lymphoid tissue, including an EBV+ analog of multipotent activated precursors that can yield early memory B cells. These resources yield exquisitely detailed perspectives of the transforming cellular landscape during an oncogenic viral infection that simulates antigen-induced B cell activation and differentiation. Thus, they support investigations of state-specific EBV-host dynamics, effector B cell fates, and lymphomagenesis. To demonstrate this potential, we identify EBV infection dynamics in FCRL4+/TBX21+ atypical memory B cells that are pathogenically associated with numerous immune disorders.
Duke Scholars
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- Transcriptome
- Humans
- Host-Pathogen Interactions
- Herpesvirus 4, Human
- Epstein-Barr Virus Infections
- B-Lymphocytes
- 31 Biological sciences
- 1116 Medical Physiology
- 0601 Biochemistry and Cell Biology
Citation
Published In
DOI
EISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Transcriptome
- Humans
- Host-Pathogen Interactions
- Herpesvirus 4, Human
- Epstein-Barr Virus Infections
- B-Lymphocytes
- 31 Biological sciences
- 1116 Medical Physiology
- 0601 Biochemistry and Cell Biology