FIG. 3.

Comparison of liver architecture of short-term (A, B, and C) and long-term (D, E, and F) HBV-infected human liver-uPA-SCID mice. Human hepatocytes (H) in short-term-infected animals have a pale appearance on H&E staining (A) due to the accumulation of glycogen as shown by PAS staining (inset). Diseased mouse hepatocytes (M) are devoid of glycogen. (B) Staining for human albumin shows that short-term infection does not compromise the functionality of the human hepatocytes. (C) PASα staining on the same livers shows that ceroid macrophages, an indication of cell loss, are confined to the diseased mouse regions. (D) The majority of long-term HBV-infected human hepatocytes have a ground-glass appearance on H&E staining, whereas these were absent in uninfected and short-term-infected livers. The insert shows a magnification of human ground-glass hepatocytes. (E) Long-term HBV infection results in an overall deterioration of the condition of the cells as shown by the decreased albumin production. (F) Large amounts of ceroid macrophages are now also present in the regions occupied by human hepatocytes, indicating that long-term infection causes the death of human hepatocytes. Original magnifications: A, C, D, and F, ×200; insets, B, and E, ×400.