Viral Induction of Low Frequency Interferon-α Producing Cells

Feldman, Stephen B.; Ferraro, Maria Grazia; Huanying, Zheng; Patel, Neil; Gould-Fogerite, Susan; Fitzgerald‐Bocarsly, Patricia

doi:10.1006/viro.1994.1504

Cited by 92 publications

(74 citation statements)

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“…This point needed to be established, however, since IFN-a/b is induced by viruses such as HSV, human immunodeficiency virus type 1 (HIV-1) and vesicular stomatitis virus (Feldman et al, 1994), which do not bind sialic acid. Furthermore, influenza virus may also interact with cells in other ways.…”

Section: Discussionmentioning

confidence: 99%

“…These so-called 'natural' IFN-producing cells (IPCs), found in human and porcine peripheral blood and mouse spleen, produce type 1 IFN in response to physically and chemically inactivated virus, to fixed virusinfected cells, or to cells transfected with particular viral glycoproteins (Fitzgerald-Bocarsly, 1993;Ito, 1994). This IFN-inducing activity has been described for a range of enveloped viruses including herpes-, lenti-, rhabdo-, corona-, orthomyxo-and paramyxoviruses and appears to result from a direct interaction of viral glycoproteins with the surface of the IPC (Charley & Laude, 1988; FitzgeraldBocarsly, 1993;Feldman et al, 1994). The principal IPC in human blood has been identified as a particular subset of immature DCs, the type 2 DC precursor or plasmacytoid DC (Cella et al, 1999;Siegal et al, 1999).…”

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confidence: 99%

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Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells

Miller

Anders

2003

Journal of General Virology

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Inactivated influenza A virus and fixed, virus-infected cells induce type 1 interferon (IFN-a/b) production in murine splenocytes. In this study, we have explored the nature of the virus-spleen cell interaction that leads to IFN-a/b induction and the reason for the poor response to some virus strains. IFN-a/b induction by horse serum-sensitive, but not -resistant, strains of influenza virus was inhibited in the presence of horse serum, indicating that binding of the virus to sialylated cell receptors is a necessary step in the induction process. Furthermore, influenza viruses A/PR/8/34 (H1N1) and A/WS/33 (H1N1), which were poor inducers of IFN-a/b in spleen cells, were shown to have a more active neuraminidase than strains that induced higher IFN levels, and IFN-a/b induction by A/PR/8/34 (H1N1) and A/WS/33 (H1N1) was restored in the presence of a neuraminidase inhibitor. Growth of virus in different cell types altered the level of IFN-a/b induced in spleen cells by particular virus strains, suggesting that the nature of the carbohydrate moieties on the viral glycoproteins may also influence IFN-a/b induction in this system. Consistent with this notion, treatment of egg-grown virus with periodate to oxidize viral carbohydrate greatly reduced its capacity for IFN-a/b induction. Furthermore, induction of IFN-a/b was inhibited in the presence of the saccharides yeast mannan and laminarin. Together these findings indicate: (i) a requirement for interaction of the virus with sialylated receptors on the IFN-producing cell; (ii) an influence of viral carbohydrate on the response; and (iii) possible involvement of a lectin-like receptor on the IFN-producing cell in the induction of IFN-a/b or in regulation of this response. INTRODUCTIONThe type 1 interferons (IFN-a and -b) are key components of antiviral host defence and modulators of the immune system. Produced within hours of viral infection, IFN-a/b induces an antiviral state in uninfected cells (Isaacs & Lindenmann, 1957) that helps to contain spread of the virus (Muller et al., 1994). IFN-a/b also activates natural killer cells and macrophages (Biron et al., 1999;Bogdan, 2000), promotes the maturation and activation of dendritic cells (DCs) (Luft et al., 1998;Gallucci et al., 1999;), and displays potent adjuvant activity for T and B cell responses in vivo (Le Bon et al., 2001).Many cell types can produce IFN-a/b in response to virus infection. Double-stranded RNA (dsRNA) synthesized during the virus replicative cycle (Jacobs & Langland, 1996) is considered a likely trigger, since synthetic dsRNA, e.g. polyinosinic-polycytidylic acid [poly(I)?poly(C)] is known to be a potent inducer of type 1 IFN (De Clercq, 1981). A second pathway of IFN-a/b induction that is independent of virus replication or gene expression is seen in the response of certain cells of haemopoietic origin to enveloped viruses. These so-called 'natural' IFN-producing cells (IPCs), found in human and porcine peripheral blood and mouse spleen, produce type 1 IFN in response to physically and chemical...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells

Miller

Anders

2003

Journal of General Virology

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“…Intriguingly, TLR9-mediated IFN-␣ secretion in response to HSV-1, HSV-2, and MCMV occurs in a MyD88-dependent manner (48,54,73), which is in direct contrast to IFN responses mediated by other TLRs, which induce IFN-␣/␤ secretion through MyD88-independent pathways. Furthermore, the TLR9-mediated IFN-␣ response to HSV-1 and HSV-2 may be limited to plasmacytoid dendritic cells (pDCs), a dendritic cell subpopulation characterized by their ability to secrete high levels of IFN in response to viral infection (7,15,20,21,24,27,63,68,70). Murine dendritic cell subsets distinct from pDCs do not secrete IFN-␣ in response to HSV-1 or HSV-2, indicating that this cell type may be specifically designed to combat viruses (48,54).…”

Section: Molecular Basis Of Tlr Activationmentioning

confidence: 99%

Innate Sensing of Viruses by Toll-Like Receptors

Boehme

Compton

2004

J Virol

234

199

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“…The main function of pDCs appears to be the production of a large amount of type I interferons (IFNs) in response to infection. [9][10][11][12] Although pDCs produce a large amount of IFN-a in response to infections, other populations of peripheral blood cells such as monocytes, B cells and mDCs can also produce IFN-a under certain conditions. In addition, IFN-a can be produced in response to a wide variety of other substances.…”

Section: Introductionmentioning

confidence: 99%

IFN-α production by human mononuclear cells infected with varicella-zoster virus through TLR9-dependent and -independent pathways

Huang

Kuo

et al. 2011

Cell Mol Immunol

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Understanding the defense mechanisms of the host of an organism is important for infection control. In previous studies, we demonstrated that interferon-a (IFN-a), but not IL-12, was produced by human peripheral blood mononuclear cells infected with varicella-zoster virus (VZV). Here, we investigated what kind of cell(s) and which signal molecule(s) are involved in IFN-a production. Using cell isolation and ELISA, we found that plasmacytoid dendritic cells (pDCs) were responsible for IFN-a production during VZV infection. We also found that Toll-like receptor 9 (TLR9) was involved in VZV-induced IFN-a production because inhibitory CpG oligodeoxynucleotide inhibited IFN-a production. UV-inactivated VZV-induced IFN-a production was lower than that of active VZV, indicating another TLR9-independent pathway. Further studies demonstrated that double-stranded RNA-dependent protein kinase, but not DNA-dependent protein kinase was involved in VZV-induced IFN-a production. Together, these results suggest that pDCs play an important role in IFN-a production during VZV infection through TLR9-dependent and -independent pathways.

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Viral Induction of Low Frequency Interferon-α Producing Cells

Cited by 92 publications

References 0 publications

Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells

Virus–cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells

Innate Sensing of Viruses by Toll-Like Receptors

IFN-α production by human mononuclear cells infected with varicella-zoster virus through TLR9-dependent and -independent pathways

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