Study Reveals Molecular Mechanism on Virus to Induce Cell Apoptosis
Apr 04, 2014 Email"> PrintText Size
As the first line of host defense, innate immunity plays an important role in the resistance of viruses and other pathogenic microorganism’s invasion. On one hand, the host cells can induce type I interferon to exert antiviral function under virus stimulation. On the other hand, the induction of apoptosis following viral infection is another effective means by which the host attempts to restrict the spread of pathogens by sacrificing the virus-infected cells. However, the underlying mechanisms are poorly understood..
Prof. WANG Chen research team from the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy
Dr. HUANG Yefeng, LIU Heng and their colleagues found that MAVS could activate type I interferon and JNK signaling. Knockdown of MAVS appeared to attenuate JNK activation and cell apoptosis during RNA virus infection. By using the MAVS, MKK7 and JNK2 knockout MEF, the study demonstrated that they were all necessary for virus induced cell apoptosis. Furthermore, MAVS could specifically interact with MKK7 and recruit it onto the mitochondria, activate the downstream JNK2, mediate cell apoptosis induced by virus. By establishing mouse model of virus infection, they found the apoptosis was significant inhibited in JNK2 knockout mouse’s lung and liver in contrast to wild-type mice. This study provides new insights for further drug design and antiviral therapy.
This study entitled “MAVS-MKK7-JNK2 Defines a Novel Apoptotic Signaling Pathway during Viral Infection” was published online in PLoS Pathogens on Mar 20, 2014. This work was supported by the grants from the Chinese Academy
Schematic diagram of the MAVS-MKK7-JNK2 apoptosis signaling pathway. (Image by Prof. WANG Chen's group)
As the first line of host defense, innate immunity plays an important role in the resistance of viruses and other pathogenic microorganism’s invasion. On one hand, the host cells can induce type I interferon to exert antiviral function under virus stimulation. On the other hand, the induction of apoptosis following viral infection is another effective means by which the host attempts to restrict the spread of pathogens by sacrificing the virus-infected cells. However, the underlying mechanisms are poorly understood..
Prof. WANG Chen research team from the
Dr. HUANG Yefeng, LIU Heng and their colleagues found that MAVS could activate type I interferon and JNK signaling. Knockdown of MAVS appeared to attenuate JNK activation and cell apoptosis during RNA virus infection. By using the MAVS, MKK7 and JNK2 knockout MEF, the study demonstrated that they were all necessary for virus induced cell apoptosis. Furthermore, MAVS could specifically interact with MKK7 and recruit it onto the mitochondria, activate the downstream JNK2, mediate cell apoptosis induced by virus. By establishing mouse model of virus infection, they found the apoptosis was significant inhibited in JNK2 knockout mouse’s lung and liver in contrast to wild-type mice. This study provides new insights for further drug design and antiviral therapy.
This study entitled “MAVS-MKK7-JNK2 Defines a Novel Apoptotic Signaling Pathway during Viral Infection” was published online in PLoS Pathogens on Mar 20, 2014. This work was supported by the grants from the
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| Schematic diagram of the MAVS-MKK7-JNK2 apoptosis signaling pathway. (Image by Prof. WANG Chen's group) |
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