Impaired germinal center formation and absence of long-lived plasma cells in chronically infected SAP^– mice. B-cell responses in wild-type and SAP^– mice chronically infected with LCMV_cl13 were measured at day 30 after infection (A-B,E-H). (A) Germinal center B cells in spleen were quantified by cytometry (Fas^hi PNA^hi IgD^– B220⁺). Germinal center responses were 30-fold larger in WT mice (P < .001) (WT, n = 13; SAP^–, n = 5). (B) Gated B cells (B220⁺) are shown. All Fas^hi PNA^hi germinal center B cells were IgD^– (not shown). Background staining was 0.2% in an uninfected B6 mouse. (C) For comparison, germinal center B cells were quantified at day 30 after acute infection with LCMV_arm. WT responses were 20-fold higher than those of SAP^– mice (P < .001). (D) Gated B220⁺ B cells are shown on day 30 after LCMV_arm infection. All Fas^hi PNA^hi germinal center B cells were IgD^– (not shown). (E) IgG⁺ virus-specific plasma cells and plasmablasts (antibody secreting cells [ASC]) in the spleen were quantified by ELISPOT on day 30 after LCMV_cl13 infection. WT responses were 9-fold higher than those of SAP^– mice (P < .01). (F) Long-lived plasma cells in the bone marrow. Anti-LCMV IgG⁺ plasma cells were quantified from the femurs using ELISPOT. Nine-fold more anti-LCMV plasma cells were present in WT bone marrow than in SAP^– bone marrow (P < .001). (G) Total IgG⁺ ASCs in spleen were 9-fold more numerous in WT than in SAP^– mice (P < .01). (H) Total IgG⁺ long-lived plasma cells in bone marrow were 8 times more prevalent in WT bone marrow than in SAP^– bone marrow (P < .001). **P < .01; ***P < .001.