Figure 2. In the absence of an intact autophagy pathway, pancreatic titers of infectious CVB3 are dramatically reduced early in infection, and pancreatic pathology is partially mitigated.

The key in panel A, showing the three lines of mice, applies also to panels B, C & E. (A & B). Mice were infected with wtCVB3 (10⁴ pfu i.p.) and, at days 1, 2, 4 and 7 p.i. the pancreata were harvested and virus titers of pancreatic homogenates were determined by plaque assay. In each group, the total number of mice used was: Atg5^f/f/Cre⁻, 52; Atg5^f/f/Cre⁺, 50; Atg5^f/wt/Cre⁺, 47. (A). Horizontal green bars indicate the geometric means, which are re-plotted in (B) to more clearly present the viral replication kinetics in each group. (C). Mice were infected with a recombinant CVB3, DsRed-CVB3 (10⁷ pfu i.p.), and pancreatic titers were measured at 2 days p.i. (D). At the indicated times p.i., histological sections were prepared from pancreata of Atg5^f/f/Cre⁻ or Atg5^f/f/Cre⁺ mice and stained with Masson’s trichrome. (E). Serum amylase levels were measured at 2 days p.i. in the indicated mouse strains. Prior to infection, the average level was ~6 U/mL.