FIG 2.

MHV68 latency alters the innate immune response to LCMV. Ten-week-old naive C57BL/6 mice were intranasally (i.n.) infected with 10⁴ PFU of MHV68 or medium. Thirty-five days postinfection, mice were challenged with serum-free RPMI or 2 × 10⁵ PFU of LCMV Armstrong intraperitoneally (i.p.). On the indicated day post-LCMV infection (A), sera were harvested, and IFN-β levels were determined by ELISA. The average and standard deviation are plotted. On day 2 postinfection, splenocytes were isolated from mock-infected mice, mice infected with LCMV or MHV68 only, or animals infected with both viruses, and the numbers of macrophages (B), natural killer (NK) (C), myeloid (D), lymphoid (F), and plasmacytoid (H) dendritic cells were determined. The fold induction relative to mock infection of maturation markers was measured for myeloid (E), lymphoid (G), and plasmactyoid (I) dendritic cells. The average and standard deviation are plotted. *, significant difference between mice infected with LCMV and mice infected with both LCMV and MHV68 (P ≤ 0.05). Six to nine mice were harvested in three independent experiments.