tetano
Editor, Senior Moderator
Heterologous SH3-p85beta inhibits influenza A virus replication
Dan-gui Zhang email, Wei-zhong Li email, Ge-fei Wang email, Yun Su email, Jun Zeng email, Chi Zhang email, Xiang-xing Zeng email, Xiao-xuan Chen email, Yan-xuan Xu email and Kang-sheng Li email
Virology Journal 2010, 7:170doi:10.1186/1743-422X-7-170
Published: 23 July 2010
Abstract (provisional)
Phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway can support the replication of influenza A virus through binding of viral NS1 protein to the Src homology 3 (SH3) domain of p85beta regulatory subunit of PI3K. Here we investigated the effect of heterologously overexpressed SH3 on the replication of different influenza A virus subtypes/strains, and on the phosphorylation of Akt in the virus-infected cells. We found that heterologous SH3 reduced replication of influenza A viruses at varying degrees in a subtype/strain-dependent manner and SH3 overexpression reduced the induction of the phosphorylation of Akt in the cells infected with PR8(H1N1) and ST364(H3N2), but not with ST1233(H1N1), Ph2246(H9N2), and Qa199(H9N2). Our results suggest that interference with the NS1-p85beta interaction by heterologous SH3 can be served as a useful antiviral strategy against influenza A virus infection.
http://www.virologyj.com/content/7/1/170
Dan-gui Zhang email, Wei-zhong Li email, Ge-fei Wang email, Yun Su email, Jun Zeng email, Chi Zhang email, Xiang-xing Zeng email, Xiao-xuan Chen email, Yan-xuan Xu email and Kang-sheng Li email
Virology Journal 2010, 7:170doi:10.1186/1743-422X-7-170
Published: 23 July 2010
Abstract (provisional)
Phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway can support the replication of influenza A virus through binding of viral NS1 protein to the Src homology 3 (SH3) domain of p85beta regulatory subunit of PI3K. Here we investigated the effect of heterologously overexpressed SH3 on the replication of different influenza A virus subtypes/strains, and on the phosphorylation of Akt in the virus-infected cells. We found that heterologous SH3 reduced replication of influenza A viruses at varying degrees in a subtype/strain-dependent manner and SH3 overexpression reduced the induction of the phosphorylation of Akt in the cells infected with PR8(H1N1) and ST364(H3N2), but not with ST1233(H1N1), Ph2246(H9N2), and Qa199(H9N2). Our results suggest that interference with the NS1-p85beta interaction by heterologous SH3 can be served as a useful antiviral strategy against influenza A virus infection.
http://www.virologyj.com/content/7/1/170