Astrovirus replication in human intestinal enteroids reveals multi-cellular tropism and an intricate host innate immune landscape
Fig 2
VA1 replication is not affected by the differentiation status of HIE.
A-B) Differentiation status of J2 and D124 HIE monitored at 0 and 6 days post-differentiation (dpd) (after WNT3A removal) by measuring transcripts of (A) down-regulated genes—LGR5 (a stem-cell marker) and Lysozyme (a Paneth cells marker), and (B) up-regulated genes—MUC2 (a goblet cell marker) and sucrase isomaltase (a mature enterocyte marker). Transcript levels were measured by qPCR. Fold change is relative to GAPDH and is statistically significantly different (P<0.05) from the 0 dpd in A) and B). C-D) VA1 replicates in HIE pre- and post- differentiation. C) D124 and D) J2 HIE were differentiated for 6 days, infected with VA1 (MOI of 1), and viral genome titers were measured at the indicated days by RT-qPCR. Fold increase was calculated by dividing 3 dpi virus titer with 0 dpi virus titer. N ≥ 3; error = mean ± SD. Abbreviations: D = duodenum, J = jejunum. The number associated with each letter indicates the patient identifier. The numbers on the bar chat indicate the fold increase in virus titer at 3 dpi over 0 dpi. NS = not significant.