Journal
CELL REPORTS
Volume 30, Issue 4, Pages 1013-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2019.12.023
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Funding
- European Research Council (ERC) [310962, 693267]
- Swiss National Science Foundation [310030_173132, 310030_173010, 323630_151472]
- SystemsX.ch-AntibodyX RTD
- Fondation Princesse Grace de Monaco
- European Research Council (ERC) [693267] Funding Source: European Research Council (ERC)
- Swiss National Science Foundation (SNF) [310030_173132, 310030_173010] Funding Source: Swiss National Science Foundation (SNF)
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Persistent viral infections subvert key elements of adaptive immunity. To compare germinal center (GC) B cell responses in chronic and acute lymphocytic choriomeningitis virus infection, we exploit activation-induced deaminase (AID) fate-reporter mice and perform adoptive B cell transfer experiments. Chronic infection yields GC B cell responses of higher cellularity than acute infections do, higher memory B cell and antibody secreting cell output for longer periods of time, a better representation of the late B cell repertoire in serum immunoglobulin, and higher titers of protective neutralizing antibodies. GC B cells of chronically infected mice are similarly hypermutated as those emerging from acute infection. They efficiently adapt to viral escape variants and even in hypermutation-impaired AID mutant mice, chronic infection selects for GC B cells with hypermutated B cell receptors (BCRs) and neutralizing antibody formation. These findings demonstrate that, unlike for CD8(+) T cells, chronic viral infection drives a functional, productive, and protective GC B cell response.
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