tetano
Editor, Senior Moderator
Oncotarget. 2017 Mar 23. doi: 10.18632/oncotarget.16503. [Epub ahead of print]
[h=1]The innate immunity of guinea pigs against highly pathogenic avian influenza virus infection.[/h] Zhang K[SUP]1,[/SUP][SUP]2[/SUP], Wei Xu W[SUP]1[/SUP], Zhang Z[SUP]1[/SUP], Liu J[SUP]1[/SUP], Li J[SUP]3[/SUP], Sun L[SUP]4[/SUP], Sun W[SUP]1[/SUP], Jiao P[SUP]5[/SUP], Sang X[SUP]1[/SUP], Ren Z[SUP]1[/SUP], Yu Z[SUP]1[/SUP], Li Y[SUP]1[/SUP], Feng N[SUP]1[/SUP], Wang T[SUP]1[/SUP], Wang H[SUP]1[/SUP], Yang S[SUP]1[/SUP], Zhao Y[SUP]1[/SUP], Zhang X[SUP]4[/SUP], Wilker PR[SUP]6[/SUP], Liu W[SUP]3[/SUP], Liao M[SUP]5[/SUP], Chen H[SUP]7[/SUP], Gao Y[SUP]1[/SUP], Xia X[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] H5N1 avian influenza viruses are a major pandemic concern. In contrast to the highly virulent phenotype of H5N1 in humans and many animal models, guinea pigs do not typically display signs of severe disease in response to H5N1 virus infection. Here, proteomic and transcriptional profiling were applied to identify host factors that account for the observed attenuation of A/Tiger/Harbin/01/2002 (H5N1) virulence in guinea pigs. RIG-I and numerous interferon stimulated genes were among host proteins with altered expression in guinea pig lungs during H5N1 infection. Overexpression of RIG-I or the RIG-I adaptor protein MAVS in guinea pig cell lines inhibited H5N1 replication. Endogenous GBP-1 expression was required for RIG-I mediated inhibition of viral replication upstream of the activity of MAVS. Furthermore, we show that guinea pig complement is involved in viral clearance, the regulation of inflammation, and cellular apoptosis during influenza virus infection of guinea pigs. This work uncovers features of the guinea pig innate immune response to influenza that may render guinea pigs resistant to highly pathogenic influenza viruses.
[h=4]KEYWORDS:[/h] GBP-1; RIG-I; guinea pig; highly pathogenic avian influenza virus; innate immunity
PMID: 28418930 DOI: 10.18632/oncotarget.16503
[h=1]The innate immunity of guinea pigs against highly pathogenic avian influenza virus infection.[/h] Zhang K[SUP]1,[/SUP][SUP]2[/SUP], Wei Xu W[SUP]1[/SUP], Zhang Z[SUP]1[/SUP], Liu J[SUP]1[/SUP], Li J[SUP]3[/SUP], Sun L[SUP]4[/SUP], Sun W[SUP]1[/SUP], Jiao P[SUP]5[/SUP], Sang X[SUP]1[/SUP], Ren Z[SUP]1[/SUP], Yu Z[SUP]1[/SUP], Li Y[SUP]1[/SUP], Feng N[SUP]1[/SUP], Wang T[SUP]1[/SUP], Wang H[SUP]1[/SUP], Yang S[SUP]1[/SUP], Zhao Y[SUP]1[/SUP], Zhang X[SUP]4[/SUP], Wilker PR[SUP]6[/SUP], Liu W[SUP]3[/SUP], Liao M[SUP]5[/SUP], Chen H[SUP]7[/SUP], Gao Y[SUP]1[/SUP], Xia X[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] H5N1 avian influenza viruses are a major pandemic concern. In contrast to the highly virulent phenotype of H5N1 in humans and many animal models, guinea pigs do not typically display signs of severe disease in response to H5N1 virus infection. Here, proteomic and transcriptional profiling were applied to identify host factors that account for the observed attenuation of A/Tiger/Harbin/01/2002 (H5N1) virulence in guinea pigs. RIG-I and numerous interferon stimulated genes were among host proteins with altered expression in guinea pig lungs during H5N1 infection. Overexpression of RIG-I or the RIG-I adaptor protein MAVS in guinea pig cell lines inhibited H5N1 replication. Endogenous GBP-1 expression was required for RIG-I mediated inhibition of viral replication upstream of the activity of MAVS. Furthermore, we show that guinea pig complement is involved in viral clearance, the regulation of inflammation, and cellular apoptosis during influenza virus infection of guinea pigs. This work uncovers features of the guinea pig innate immune response to influenza that may render guinea pigs resistant to highly pathogenic influenza viruses.
[h=4]KEYWORDS:[/h] GBP-1; RIG-I; guinea pig; highly pathogenic avian influenza virus; innate immunity
PMID: 28418930 DOI: 10.18632/oncotarget.16503