Concentration and purification of influenza virus from allantoic fluid

Arora, D. J. S.; Tremblay, Pierre; Bourgault, Richard; Boileau, Serge

doi:10.1016/0003-2697(85)90103-4

Cited by 47 publications

(21 citation statements)

References 6 publications

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“…Viral particles were purified by sucrose density gradient centrifugation (Arora et al, 1985; Hartshorn et al, 1988, 1997) and quantitated using a fluorescent focus assay of influenza A virus infection as previously described (van Eijk et al, 2003). Briefly, MDCK cell monolayers were prepared in 96 well plates and grown to confluency.…”

Section: Methodsmentioning

confidence: 99%

GM-CSF modulates pulmonary resistance to influenza A infection

et al. 2011

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Alveolar type II epithelial or other pulmonary cells secrete GM-CSF that regulates surfactant catabolism and mucosal host defense through its capacity to modulate the maturation and activation of alveolar macrophages. GM-CSF enhances expression of scavenger receptors MARCO and SR-A. The alveolar macrophage SP-R210 receptor binds the surfactant collectin SP-A mediating clearance of respiratory pathogens. The current study determined the effects of epithelial-derived GM-CSF in host resistance to influenza A pneumonia. The results demonstrate that GM-CSF enhanced resistance to infection with 1.9 × 104 ffc of the mouse-adapted influenza A/Puerto Rico/8/34 (PR8) H1N1 strain, as indicated by significant differences in mortality and mean survival of GM-CSF-deficient (GM−/−) mice compared to GM−/− mice in which GM-CSF is expressed at increased levels. Protective effects of GM-CSF were observed both in mice with constitutive and inducible GM-CSF expression under the control of the pulmonary-specific SFTPC or SCGB1A1 promoters, respectively. Mice that continuously secrete high levels of GM-CSF developed desquamative interstitial pneumonia that impaired long-term recovery from influenza. Conditional expression of optimal GM-CSF levels at the time of infection, however, resulted in alveolar macrophage proliferation and focal lymphocytic inflammation of distal airways. GM-CSF enhanced alveolar macrophage activity as indicated by increased expression of SP-R210 and CD11c. Infection of mice lacking the GM-CSF-regulated SR-A and MARCO receptors revealed that MARCO decreases resistance to influenza in association with increased levels of SP-R210 in MARCO−/− alveolar macrophages. In conclusion, GM-CSF enhances early host resistance to influenza. Targeting of MARCO may reinforce GM-CSF-mediated host defense against pathogenic influenza.

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Section: Methodsmentioning

confidence: 99%

GM-CSF modulates pulmonary resistance to influenza A infection

et al. 2011

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“…Virus containing allantoic fluid was harvested, aliquoted and frozen at −80°C until used in experiments. Purified virus was prepared by equilibrium and differential sucrose density gradient separations [51]. VN/04 virus was used in animal challenge experiments and for the isolation of viral RNA.…”

Section: Methodsmentioning

confidence: 99%

Induction of Long-Term Protective Immune Responses by Influenza H5N1 Virus-Like Particles

et al. 2009

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BackgroundRecurrent outbreaks of highly pathogenic H5N1 avian influenza virus pose a threat of eventually causing a pandemic. Early vaccination of the population would be the single most effective measure for the control of an emerging influenza pandemic.Methodology/Principal FindingsInfluenza virus-like particles (VLPs) produced in insect cell-culture substrates do not depend on the availability of fertile eggs for vaccine manufacturing. We produced VLPs containing influenza A/Viet Nam1203/04 (H5N1) hemagglutinin, neuraminidase, and matrix proteins, and investigated their preclinical immunogenicity and protective efficacy. Mice immunized intranasally with H5N1 VLPs developed high levels of H5N1 specific antibodies and were 100% protected against a high dose of homologous H5N1 virus infection at 30 weeks after immunization. Protection is likely to be correlated with humoral and cellular immunologic memory at systemic and mucosal sites as evidenced by rapid anamnestic responses to re-stimulation with viral antigen in vivo and in vitro.Conclusions/SignificanceThese results provide support for clinical evaluation of H5N1 VLP vaccination as a public health intervention to mitigate a possible pandemic of H5N1 influenza.

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“…Virus stocks were grown in the chorioallantoic fluid of 10-d-old embryonated hen's eggs, and purified on a discontinuous sucrose density gradient as previously described (21,22). Virus stocks were suspended in Dulbecco's modified phosphate-buffered saline (PBS), aliquoted and stored at -70'C until used.…”

Section: Methodsmentioning

confidence: 99%

Evidence for a protective role of pulmonary surfactant protein D (SP-D) against influenza A viruses.

Hartshorn

Crouch²,

White³

et al. 1994

J. Clin. Invest.

304

343

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We tested the hypothesis that pulmonary surfactant-associated lectins -surfactant proteins A and D (SP-A, and -D) contribute to initial protective mechanisms against influenza A viruses (IAVs). SP-D potently inhibited hemagglutination activity of several strains of IAV as well as causing viral aggregation. SP-D enhanced neutrophil binding of 1AV and neutrophil respiratory burst responses to the virus. Neutrophil dysfunction resulting from 1AV exposure was diminished when the virus was pre-incubated with SP-D. Each of these effects was mediated by the calcium-dependent carbohydrate-binding property of SP-D. Native SP-D preparations of both human and rat origin, as well as recombinant rat SP-D, had similar activity. SP-A also inhibited IAV hemagglutination activity. We have previously reported that related mammalian serum lectins (mannose-binding lectin [MBL] and conglutinin) have similar effects. SP-D was at least 10-fold more potent at causing hemagglutination inhibition than were SP-A or MBL. SP-D was shown to contribute to potent anti-IAV activity of human bronchoalveolar lavage fluid. These results suggest that SP-D-alone, and in conjunction with SP-A and phagocytic cells-constitutes an important component of the natural immune response to 1AV infection within the respiratory tract. (J. Clin. Invest.

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Concentration and purification of influenza virus from allantoic fluid

Cited by 47 publications

References 6 publications

GM-CSF modulates pulmonary resistance to influenza A infection

GM-CSF modulates pulmonary resistance to influenza A infection

Induction of Long-Term Protective Immune Responses by Influenza H5N1 Virus-Like Particles

Evidence for a protective role of pulmonary surfactant protein D (SP-D) against influenza A viruses.

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