期刊
VIROLOGY
卷 400, 期 1, 页码 104-114出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2010.01.024
关键词
Avian reovirus S1333; Pro-inflammatory cytokine; Apoptosis; PI 3-kinase
类别
资金
- National Science Council [NSC-96-2313B-320-001]
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. (C) 2010 Published by Elsevier Inc.
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