Autophagy and apoptosis are two of main processes involved in maintenance of cellular homeostasis as well as the innate immune defense. Herpes simplex virus type 1 (HSV-1) is known to regulate both processes. Recent studies have demonstrated that viral gene US11 is involved in control of autophagy. In order to demonstrate if there may be a crosstalk between both processes, we enrolled HSV-1 and a mutant virus R7023, with a deletion including US11 gene, to analyze autophagy and apoptosis markers. We observed that in THP-1 wt cell lines there was an activation of autophagy after infection of mutant virus R7023, but not with HSV-1. Recent studies have shown that Beclin-1, an autophagic marker, is degraded by caspase-8, which colocalizes with p62 protein on the surface of autophagosomes membrane. Activation of caspase-8 is regulated by FLIP protein. We observed that in cells infected with HSV-1, but not with mutant virus, there was a degradation of FLIP at 24, 48, 72 h.p.i. corresponding to an activation of caspase-8, that could lead to a blockage of autophagy. Based on these data we have obtained evidences about the interplays between autophagy and apoptosis pathways during viral replication.
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