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. 2015 Aug 15;25(5):634–650. doi: 10.1111/bpa.12281

Figure 8.

figure

HPeV3 infects blood vessel smooth muscle cells in leptomeninges and pulmonary vasculature. A,B. Paraffin‐embedded cerebellum and overlying leptomeninges probed for HPeV3 RNA using in situ hybridization (red) (counterstained with hematoxylin). Abundant HPeV3 viral RNA is confined to the modestly hypercellular leptomeninges with no evidence of infection of the brain parenchyma. Higher power (B) image of (A) confirms the presence of HPeV3 RNA in leptomeningeal cells and particularly in smooth muscle cells of blood vessel walls. C,D. Paraffin‐embedded lung probed for HPeV3 RNA using in situ hybridization (red) (counterstained with hematoxylin). HPeV3 RNAs are confined to the modestly hypercellular pulmonary arteries without evidence of lung parenchymal infection. Higher power (D) of (C) confirms the presence of HpeV3 RNA in smooth muscle cells of blood vessel walls. These observations suggest that damage noted in severe periventricular leukoencephalopathy is an indirect effect of vascular compromise to metabolically active regions.