Activation of PI 3-kinase/Akt/NF-kappa B and Stat3 signaling by avian reovirus S1133 in the early stages of infection results in an inflammatory response and delayed apoptosis

作者：Lin Ping Yuan; Liu Hung Jen; Liao Ming Huei; Chang Ching Dong; Chang Chi I; Cheng Hsueh Ling; Lee Jeng Woei; Shih Wen Ling^*

来源：Virology, 2010, 400(1): 104-114.

DOI：10.1016/j.virol.2010.01.024

• Avian reovirus S1333
• Pro-inflammatory cytokine
• Apoptosis
• PI 3-kinase

Avian reovirus (ARV) strain S1133 causes apoptosis in host cells in the middle to late stages of infection. This study investigated the early-stage biological response and intracellular signaling in ARV S1133-infected Vero and chicken cells. Treatment with conditioned medium from ARV S1133-infected cells increased the chemotactic activity of U937 cells. Neutralizing antibodies against IL-1 beta and IL-6 showed that both cytokines contribute to Viral-induced inflammation but neither affect cell survival. Inhibition of Akt, NF-kappa B, and Stat3 released the chemotactic activity and anti-apoptotic effect elicited by ARV S1133. ARV S1133 activated PI 3-kinase-dependent Akt/NF-kappa B and p70 S6 kinase, as well as Stat3: however, p70 S6 kinase was not involved in ARV S1133-mediated effects. DF1 cells over-expressing constitutively active PI 3-kinase and Stat3 showed association with enhancement of anti-apoptotic activity. In conclusion, in the early stages of ARV S 1133 infection, activation of cell Survival Signals contributes to virus-induced inflammation and anti-apoptotic response.

• 出版日期2010-4-25