•Knockdown of prosurvival Mcl-1 reduces virus titer not by translation or genome replication.
•It may be due to a defect in virion assembly possibly due to capsid protein cleavage from activated caspases (Capsid of feline calicivirus and mink disease virus are cleaved by caspases)
Findings in a glance:
•F1: BeAn infected cell mostly go through necrosis, while 20% goes through apoptosis. The release of ROS is significantly increased at 10hpi and 12hpi in BeAn infected cell comparing to mock infected cell.
•F2: They saw that the prosurvival Mcl-1 is decreased during infection.
*It is strange that F2C and F2D Mcl-1 levels are not the same. It looks like 24hpi from F2C is higher than 12hpi from F2D
•F3: Knockdown of Mcl-1 reduces the BeAn titer.
•F4: They derived stable cell line with lowered Mcl-1. They showed an earlier activation of caspase 9 and caspase 3
•F5: The reduction of titer is not due to translation or genome replication defect, shown by northern blot analysis, pulse-chase
•F6:BeAn infection increases expression of p53, activates p53, Noxa and Bax
•F7: They also saw necrosis in oligodendrocytes.