| First Author | Fallet B | Year | 2020 |
| Journal | Cell Rep | Volume | 30 |
| Issue | 4 | Pages | 1013-1026.e7 |
| PubMed ID | 31995746 | Mgi Jnum | J:288089 |
| Mgi Id | MGI:6415862 | Doi | 10.1016/j.celrep.2019.12.023 |
| Citation | Fallet B, et al. (2020) Chronic Viral Infection Promotes Efficient Germinal Center B Cell Responses. Cell Rep 30(4):1013-1026.e7 |
| abstractText | 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. |
