FIG 5.
NrHV mouse-adaptive mutations do not compensate for species-specific differences in SR-BI interaction. (A) Infection of WT+/+, heterozygous+/−, or SR-BI−/− knockout mice with 106 GE of NrHV-B virus derived from rat serum (week 1 post-intrahepatic infection). The age of mice in this experiment was 9 to 15 months (mean, 11 months). (B) Infection of WT+/+, heterozygous+/−, or SR-BI−/− knockout mice with 104 GE of NrHV-BSLIS virus derived from mouse serum. Data in this panel were previously published (15) but are included here for direct comparison. The age of mice in this experiment was 2 months. (C) Immunoblot detection of SR-BI in total liver protein extracts prepared from WT+/+, heterozygous+/−, or SR-BI−/− knockout mice, demonstrating the absence of immunoreactive SR-BI in knockout mouse liver. (D) Percentage neutralization of RHVcc-1, RHVcc-2, NrHV-B (second experiment stock), or NrHV-BSLIS (see Table 1 for changes to viral ORF) using rat sera with low (R14), medium (R6), or high (R16) neutralization potential against RHVcc-1, as previously determined (15). Comparison was made in triplicate against naive preinfection sera from R16 (all sera at week 45 postinfection).