Induction of interferon by virus glycoprotein(s) in lymphoid cells through interaction with the cellular receptors via lectin-like action: An alternative interferon induction mechanism

Ito, Yoshihiro

doi:10.1007/bf01379125

Cited by 21 publications

(13 citation statements)

References 80 publications

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“…In a collaborative study with M. O'Keeffe, K. Shortman and others, we have confirmed responsiveness of purified splenic plasmacytoid pre-DCs to BPL-inactivated influenza virus and shown a lack of response to poly(I)?poly(C) (O'Keeffe et al, 2002), consistent with previous studies indicating that the viral stimulus for the splenic IPC is provided by the viral glycoproteins rather than by dsRNA (Fitzgerald-Bocarsly, 1993;Ito, 1994). The ability to work with defined populations of murine plasmacytoid pre-DCs should facilitate further study of the triggering receptor(s) and possible inhibitory receptor(s) involved in the IFN-a/b response to inactivated influenza virus and the existence of common or distinct pathways of stimulation by other enveloped viruses and microbial stimuli.…”

Section: Discussionsupporting

confidence: 89%

“…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 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).…”

Section: Introductionmentioning

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: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

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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“…The study was prompted by the work of Ito and colleagues, who showed that the binding of viral Gs to mammalian spleen cells induced these cells to produce IFN-␣/␤ (20,22). Ito and his colleagues also showed that mice given an intravenous injection of isolated viral Gs of purified Sendai virus produced 3 PFU/ml at dpc: 10 5 PFU/ml at dpc: a Mx expression for fish exposed to 10 3 or 10 5 PFU of IHNV per ml at 0, 1, 2, 5, and 7 dpc is shown.…”

Section: Discussionmentioning

confidence: 99%

“…This protein appears to be present in all vertebrate species and has been found in humans (1,18), rats (35,36), sheep (8), pigs (37), ducks (3), chickens (4), perch (43), and trout (44). Although double-stranded RNA is the best-characterized inducer of IFN, it has been proposed that expression of viral Gs also induces IFN via lectin-like activity similar to concanavalin A and phytohemagglutinin, which induce IFN in lymphoid cells (20). This response was only seen when the viral G was expressed on the surface of a host cell and was not seen in response to extracellular G. To date, IFN has not been cloned from a fish, but the detection of IFN-like activity has been well documented (16).…”

Section: Discussionmentioning

confidence: 99%

DNA Vaccines Encoding Viral Glycoproteins Induce Nonspecific Immunity and Mx Protein Synthesis in Fish

Kim

Johnson

Drennan

et al. 2000

J Virol

162

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Protective immunity by vaccination with plasmid DNA encoding a viral glycoprotein (G) has long been assumed to result from the induction of a specific immune response. We report here that the initial protection may be due to the induction of alpha/beta interferon, with long-term protection due to a specific response to the encoded viral G. DNA vaccines encoding the Gs of three serologically unrelated fish rhabdoviruses were used to vaccinate rainbow trout against a lethal challenge with infectious hematopoietic necrosis virus (IHNV). All three vaccines, each encoding the G gene of either IHNV (IHNV-G), snakehead rhabdovirus (SHRV) (SHRV-G), or spring viremia of carp virus (SVCV) (SVCV-G), elicited protective immunity against IHNV. Vaccinated fish were challenged at 30 or 70 days postvaccination with lethal doses of IHNV. At 30 days postvaccination, only 5% of fish that had received any of the G vaccines died, whereas more than 50% of the control fish succumbed to virus challenge. When fish were vaccinated and challenged at 70 days postvaccination, only 12% of the IHNV-G-vaccinated fish died compared to 68% for the SHRV-G-and 76% for the SVCV-G-vaccinated fish. Assays for trout Mx protein, an indicator of alpha/beta interferon induction, showed that only fish vaccinated with a G-containing plasmid produced high levels of Mx protein in the kidneys and liver. Interestingly, at day 7 after virus challenge, all of the fish vaccinated with the IHNV-G plasmid were negative for Mx, but the SHRV-G-and SVCV-G-vaccinated fish still showed detectable levels of Mx. These results suggest that DNA vaccines in fish induce an early, nonspecific antiviral protection mediated by an alpha/beta interferon and, later, a specific immune response.Antiviral DNA vaccines carrying a gene for a major antigenic viral protein have received considerable attention as a new approach to vaccine development, especially when traditional vaccines have failed. They offer the advantage of mimicking a viral infection, resulting in host production of a single viral protein that is correctly folded and modified, and eliciting both cellular and humoral immune responses (9, 48). DNA vaccines have been developed for a wide variety of viruses, including influenza virus (14, 46), human immunodeficiency virus (7,15,42), rabies virus (38), hepatitis B virus (10), rubella virus (41), and foot-and-mouth disease virus (19). Genetic vaccines have also been developed for several other pathogens, including Mycoplasma pulmonis (29), Mycobacterium tuberculosis (34), Plasmodium yoelii (17), and Schistosoma japonicum (49).For fish viruses, DNA vaccines have been developed for infectious hematopoietic necrosis virus (IHNV) (2, 33) and viral hemorrhagic septicemia virus (6), both rhabdoviruses belonging to the Novirhabdovirus genus. Laboratory trials with fish indicate that these vaccines are considerably more effective in protecting fish from lethal challenge with homologous virus than either the traditional killed vaccine or the subunit vaccine we had developed previous...

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“…Rogel-Gaillard et al (1993) previously reported that rainbow trout AK leucocytes and peripheral blood leucocytes produced ILC activity after stimulation by glutaraldehyde-fixed VHS virusinfected cells: Yields of ILC induced by CMA virus were similar to yields induced by free infectious and free inactivated virus (P-propiolactone-treated), although no dose-response trials were done to determine optimal MO1 for peak yields. Rogel-Gaillard et al further demonstrated that the ILC response to CMA VHS virus was abolished by treatment of fixed infected cells with a rnonoclonal antibody to the transmembrane viral glycoprotein G. It has been known for some time that interaction of human lymphocytes with fixed ceii membranes bearing viral antigens can be an adequate stimulus for IFN production (reviewed by Ito 1994), and recent research has shown that human monocytes and macrophages can also be stimulated to produce IFN-a and IFN-P by contact with fixed infected cells or with recombinant viral envelope glycoproteins (Francis & Meltzer 1993, Gessani el al. 1994).…”

Section: Discussionmentioning

confidence: 99%

Interferon-like activity produced by anterior kidney leucocytes of rainbow trout stimulated in vitro by infectious hematopoietic necrosis virus or Poly I:C

Congleton¹,

Sun²

1996

Dis. Aquat. Org.

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Leucocytes from the anterior ludneys of rainbow trout Oncorhynchus rnykiss produced an interferon-like cytokine (ILC) or cytokines when stimulated wlth free infectious hematopoietic necrosls (IHN) virus, with cell membrane-associated (CMA) IHN virus on glutaraldehyde-fixed chinook salmon embryo cells, or with the synthetic polyribonucleotide Poly 1:C. Peak yields of ILC were similar in leucocyte cultures stimulated by free virus or by CMA virus at optlrnal multiplicities of infection. The antiviral activity had both acid-resistant and acid-labile components, indicating production of several cytokines. Moreover, activity produced by free virus-stimulated leucocytes was significantly (p I 0.05) more resistant to treatment at pH 2 than was activity produced by CMA virus-stimulated leucocytes. Leucocyte populations enriched for macrophages (but not for neutrophils or lymphocytes) demonstrated a significantly enhanced capacity for ILC production after stimulation by Poly 1:C or free IHN virus. The capacity of macrophages for ILC production may be a n important element of the nonspecific resistance of salmonids to IHN virus.

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Induction of interferon by virus glycoprotein(s) in lymphoid cells through interaction with the cellular receptors via lectin-like action: An alternative interferon induction mechanism

Cited by 21 publications

References 80 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

DNA Vaccines Encoding Viral Glycoproteins Induce Nonspecific Immunity and Mx Protein Synthesis in Fish

Interferon-like activity produced by anterior kidney leucocytes of rainbow trout stimulated in vitro by infectious hematopoietic necrosis virus or Poly I:C

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