tetano
Editor, Senior Moderator
Viral Immunol. 2017 Apr 12. doi: 10.1089/vim.2016.0140. [Epub ahead of print]
[h=1]Antiviral Effect of IDO in Mouse Fibroblast Cells During Influenza Virus Infection.[/h] Li F[SUP]1,[/SUP][SUP]2[/SUP], Karlsson H[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] While upregulation of 2,3-dioxygenase (IDO) accompanied by degradation of tryptophan along the kynurenine pathway have been reported to exert antimicrobial effects against a wide range of infectious agents, its role in the replication of influenza A virus remains uncertain. We performed experiments using influenza A/WSN/33 virus infection of mouse fibroblast cell-line (NIH-3T3) to study the effects of IDO on viral replication. Influenza infection resulted in prominent elevations of transcripts encoding IDO, interferon (IFN)-β, and segment 8 of the virus in NIH-3T3 cells. Introduction of siRNA targeted against IDO followed by infection resulted in further increased levels of viral RNA without altering IFN-β expression. Inhibition of IDO during the infection also resulted in reduction of virus-driven upregulation of 3-hydroxyanthranilate 3,4-dioxygenase (HAAO), but not kynurenine 3-monooxygenase (KMO), which are enzymes downstream in the kynurenine pathway. Thus, induction of IDO appears to contribute to limiting replication of the WSN/33 strain of influenza A virus in murine NIH-3T3 cells.
[h=4]KEYWORDS:[/h] 2,3-dioxygenase; antiviral effect; influenza A/WSN/33 virus
PMID: 28402179 DOI: 10.1089/vim.2016.0140
[h=1]Antiviral Effect of IDO in Mouse Fibroblast Cells During Influenza Virus Infection.[/h] Li F[SUP]1,[/SUP][SUP]2[/SUP], Karlsson H[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] While upregulation of 2,3-dioxygenase (IDO) accompanied by degradation of tryptophan along the kynurenine pathway have been reported to exert antimicrobial effects against a wide range of infectious agents, its role in the replication of influenza A virus remains uncertain. We performed experiments using influenza A/WSN/33 virus infection of mouse fibroblast cell-line (NIH-3T3) to study the effects of IDO on viral replication. Influenza infection resulted in prominent elevations of transcripts encoding IDO, interferon (IFN)-β, and segment 8 of the virus in NIH-3T3 cells. Introduction of siRNA targeted against IDO followed by infection resulted in further increased levels of viral RNA without altering IFN-β expression. Inhibition of IDO during the infection also resulted in reduction of virus-driven upregulation of 3-hydroxyanthranilate 3,4-dioxygenase (HAAO), but not kynurenine 3-monooxygenase (KMO), which are enzymes downstream in the kynurenine pathway. Thus, induction of IDO appears to contribute to limiting replication of the WSN/33 strain of influenza A virus in murine NIH-3T3 cells.
[h=4]KEYWORDS:[/h] 2,3-dioxygenase; antiviral effect; influenza A/WSN/33 virus
PMID: 28402179 DOI: 10.1089/vim.2016.0140