MHV-A59 induced optic neuritis in a mean of 55.6% of optic nerves in 4 experiments, whereas MHV-2 induced optic neuritis in only 3.7% of optic nerves (Fig. 1G) ; this result is similar to the incidence in prior studies (8) . RSA59infected mice developed optic neuritis with a high incidence (68.5%) similar to that in MHV-A59-infected mice, and significantly higher than the incidence in RSMHV-2 infected mice (25.1%) (Fig. 1H) . Serial sections from RSA59-and RSMHV2-infected mice were stained with anti-CD45 (leukocyte common antigen; LCA), antiYIba-1 (microglia/macrophage marker), anti-CD3 (T-cell marker), or anti-CD19 (B-cell marker) (Table) . LCA staining confirmed the presence of infiltrating inflammatory cells in optic nerves from RSA59-infected mice, whereas few LCA-positive cells were found in those of RSMHV2-infected mice (not shown). Among the LCA-positive inflammatory cells, the majority in the RSA59-infected mice were Iba-1+ microglia/macrophages (Fig. 2C) . The optic nerves of some control mice (Fig. 2) and RSMHV2-infected mice (Fig. 2B ) also had scattered Iba1+ cells that likely represent resident microglia, but there were far fewer than in the RSA59-infected samples. This result was confirmed by 2 blinded investigators. Significantly more optic nerves from RSA59-infected mice had increased Iba1+ cells versus nerves from RSMHV2-infected mice (14/23 total nerves from 4 experiments versus 4/20, respectively; p = 0.0124 by Fisher exact test).