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. 2005 Mar;79(6):3267–3276. doi: 10.1128/JVI.79.6.3267-3276.2005

FIG. 6.

FIG. 6.

Virus replication defects of E1A null and CR3Δ mutants in mice. (A) Four strains of mice (SJL/J, BALB/c, 129 Sv/Ev, and IFNAR−/−) were infected by the i.p. route with wt MAV-1, E1A null mutant, or CR3Δ at 100 PFU. Brains were harvested at 8 days p.i., and homogenates were titrated for viruses by plaque assays of 37.1 cells. Each symbol represents an individual mouse. The dotted line at 2 × 103 represents the lower limit of detection of the assay. Data points below the limit of detection were excluded from statistical calculations. *, P < 0.0001 and P = 0.002 for E1A null mutant titers compared to wt MAV-1 titers in SJL/J and 129 Sv/Ev mice, respectively; **, P = 0.0001, P = 0.02, and P = 0.003 for CR3Δ titers compared to wt MAV-1 titers in SJL/J, 129 Sv/Ev, and IFNAR−/− mice, respectively. (B) SJL/J mice were infected by the i.p. route with wt MAV-1, E1A null mutant, or CR3Δ at 100 PFU. Brains were harvested at 8 days p.i. Total RNA was isolated, and RPAs were carried out with probe sets as described for the results shown in Fig. 4.