Objective To establish an LCMV-CL13 chronic infection mouse model and analyze its use for B cell somatic hypermutation research. Methods C57BL/ 6N mice were inoculated with 2×10⁶ plaque-forming units of LCMV- CL13 virus via tail vein injection. The tissue viral load was then detected by quantitative polymerase chain reaction on days 10, 20, 30, 40, 50, 60, and 70 post-infection. The CD4⁺ and CD8⁺T cell and CD19⁺ B cell ratios in peripheral blood and the germinal center B cell percentage of the spleen were determined by flow cytometry, and the gene abundance and BCR V region mutation rate were analyzed using immune repertoire technology. Results LCMV-CL13-infected mice maintained a tissue viral load of 1×10⁶ copies/ μL virus. The percentage of CD4⁺ T cells in the peripheral blood gradually increased in the infection plateau phase to ( 13. 15% ± 0. 72%), while the percentage of CD8⁺ T cells first decreased to ( 2. 17% ± 0. 40%) and then gradually recovered to (6. 65% ± 0. 52%), and the percentages of CD19⁺ B cells and germinal center B cells increased to (40. 32% ± 0. 46%) and (10. 03% ± 0. 60%), respectively. Sequencing result demonstrated that the frequency of V gene usage decreased and the mutation rate of the heavy chain CDR3 V gene increased 1. 7-fold with increasing infection time. Conclusions We successfully established a LCMV-CL13 chronic infection mouse model. This model can be used to study BCR mutations, and provides a research tool for investigating B cell somatic hypermutation caused by chronic viral infection.