tailieunhanh - Báo cáo y học: "Heterologous SH3-p85b inhibits influenza A virus replication"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Heterologous SH3-p85b inhibits influenza A virus replication | Zhang et al. Virology Journal 2010 7 170 http content 7 1 170 VIROLOGY JOURNAL RESEARCH Open Access Heterologous SH3-p85p inhibits influenza A virus replication Dan-gui Zhang1 Wei-zhong Li Ge-fei Wang Yun Su Jun Zeng Chi Zhang Xiang-xing Zeng Xiao-xuan Chen Yan-xuan Xu Kang-sheng Li Abstract Phosphatidylinositol 3-kinase PI3K Akt signalling pathway can support the replication of influenza A virus through binding of viral NS1 protein to the Src homology 3 SH3 domain of p85p regulatory subunit of PI3K. Here we investigated the effect of heterologously overexpressed SH3 on the replication of different influenza A virus sub-types 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-p85b interaction by heterologous SH3 can be served as a useful antiviral strategy against influenza A virus infection. Background Influenza A viruses are globally important human and animal respiratory pathogens and viral infections cause highly contagious respiratory diseases. Influenza A virus can be divided into numerous subtypes H1 H16 and N1 N9 according to the antigenicity of hemagglutinin HA and neuraminidase NA . Among them H1N1 and H3N2 subtypes are the most common subtype in human influenza infections 1 . However in some situations several avian influenza virus subtypes such as H5N1 H7N7 or H9N2 can break through the species barrier and be transmitted to humans 2 . These avian influenza viruses have posed serious threat to public health. One of the main research emphases in the influenza A virus is its NS1 protein. NS1 can modulate virus infection and host cell signalling pathway 3-6 such as