Interaction of Influenza Virus with Leukocytes and Its Effect on Phagocytosis

Sawyer, William D.

doi:10.1093/infdis/119.6.541

Cited by 76 publications

(47 citation statements)

References 27 publications

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“…Functional defects, including impaired phagocytosis by murine macrophages, have been observed in influenza, Sendai and cytomegalovirus infections (Sawyer, 1969;Jakab et al, 1980;Shanley & Pesanti, 1982). In Sendai virus-infected mice maximum suppression of Fc-mediated ingestion of EA by alveolar macrophages is seen 7 days after virus infection , whereas in DV-infected mice it is seen on the 4th day.…”

Section: Discussionmentioning

confidence: 99%

Effect of Dengue Virus Infection on Fc-receptor Functions of Mouse Macrophages

Chaturvedi¹,

Nagar²,

Mathur³

1983

Journal of General Virology

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Section: Discussionmentioning

confidence: 99%

Effect of Dengue Virus Infection on Fc-receptor Functions of Mouse Macrophages

Chaturvedi¹,

Nagar²,

Mathur³

1983

Journal of General Virology

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“…NWS/33 virus has been reported to possess low NA activity (Sawyer, 1969;Sedmak & Grossberg, 1973). Since we had shown an interaction with sialylated receptors is necessary for IFN-a/b induction in splenic IPCs, we investigated whether a difference in strength of the viral NA activity may account for the difference between high-and low-inducing strains of virus.…”

Section: Role Of Viral Na Activity In Ifn-a/b Induction By Influenza 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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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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“…These include a decreased clearance ability of the respiratory tract owing to damage of the ciliated epithelial cells (19,20) and decreased phagocytic ability of pulmonary macrophages (21,22). Giordano and Morrow (23) reported a depressed mucociliary transport in the respiratory tract of rats exposed to 6 ppm NO2 for 6 weeks.…”

Section: Discussionmentioning

confidence: 99%