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Abstract B lymphocyte response patterns vary in different infection scenarios, such as acute or chronic infections. This study aims to construct recombinant Armstrong and Clone13 strains of lymphocytic choriomeningitis virus (LCMV) to induce the immune response of KL25HL B cells carrying the transgenic B cell receptor (BCR) specific to the glycoprotein (GP) of the WE strain, thereby establishing a model for comparing host B cell immune response differences between acute and chronic infection processes. Firstly, by co-transfecting cells with plasmids to transcribe LCMV genome fragments and express viral proteins, recombinant LCMV-Armstrong (rARM) and recombinant LCMV-Clone13 (rCL13) were successfully rescued. Sequencing analysis results indicated that the GP sequences of these two recombinant viruses were accurately replaced with the GP sequence of the LCMV-WE strain, and they were confirmed to have plaque-forming ability after infecting cells. For further characterizing the properties of rARM and rCL13, they were used to infect C57BL/6J mice. The results suggested that these two recombinant viruses retained the acute or chronic infection properties of wild type LCMV-Armstrong (wtARM) or wild type LCMV-Clone13 (wtCL13) strains. Specifically, after establishing infection, rARM would be rapidly cleared by the host immune system within a week, while rCL13 would persist in the host for more than two months. Finally, wild-type mice adoptively transferred with KL25HL B cells were infected with different LCMV strains to study the immune response. The results showed that, compared with wtARM or wtCL13, infection with rARM or rCL13 could significantly induce the activation and proliferation of KL25HL B cells. The rARM and rCL13 constructed in this study, after infecting mice that were adoptively transferred with KL25HL B cells, could serve as a powerful tool for comparative research on B lymphocyte response patterns in acute and chronic infections, which is of great significance for deepening understanding of humoral immune response mechanisms.
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Received: 28 November 2023
Published: 01 January 2023
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