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Highly pathogenic avian influenza virus infection of mallards with homo- and heterosubtypic immunity induced by low pathogenic avian influenza viruses.

Fereidouni SR, Starick E, Beer M, Wilking H, Kalthoff D, Grund C, Häuslaigner R, Breithaupt A, Lange E, Harder TC - PLoS ONE (2009)

Bottom Line: The potential role of wild birds as carriers of highly pathogenic avian influenza virus (HPAIV) subtype H5N1 is still a matter of debate.In mallards with homosubtypic immunity induced by LPAIV infection, clinical disease was absent and shedding of HPAIV from respiratory and intestinal tracts was grossly reduced compared to the heterosubtypic and control groups (mean GEC/100 microl at 3 dpi: 3.0 x 10(2) vs. 2.3 x 10(4) vs. 8.7 x 10(4); p<0.05).We conclude that the epidemiology of HPAIV H5N1 in mallards and probably other aquatic wild bird species is massively influenced by interfering immunity induced by prior homo- and heterosubtypic LPAIV infections.

View Article: PubMed Central - PubMed

Affiliation: Friedrich-Loeffler-Institut (FLI), Insel Riems, Germany. sasan.fereidouni@fli.bund.de

ABSTRACT
The potential role of wild birds as carriers of highly pathogenic avian influenza virus (HPAIV) subtype H5N1 is still a matter of debate. Consecutive or simultaneous infections with different subtypes of influenza viruses of low pathogenicity (LPAIV) are very common in wild duck populations. To better understand the epidemiology and pathogenesis of HPAIV H5N1 infections in natural ecosystems, we investigated the influence of prior infection of mallards with homo- (H5N2) and heterosubtypic (H4N6) LPAIV on exposure to HPAIV H5N1. In mallards with homosubtypic immunity induced by LPAIV infection, clinical disease was absent and shedding of HPAIV from respiratory and intestinal tracts was grossly reduced compared to the heterosubtypic and control groups (mean GEC/100 microl at 3 dpi: 3.0 x 10(2) vs. 2.3 x 10(4) vs. 8.7 x 10(4); p<0.05). Heterosubtypic immunity induced by an H4N6 infection mediated a similar but less pronounced effect. We conclude that the epidemiology of HPAIV H5N1 in mallards and probably other aquatic wild bird species is massively influenced by interfering immunity induced by prior homo- and heterosubtypic LPAIV infections.

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Histopathology and immunohistochemistry of brain from infected ducks.(A) Brain, Cerebrum; Duck at 5 dpc. Congestion shown by hematoxylin-eosin staining. Bar 100 µm. (B) Brain, Cerebrum; Duck at 6 dpc. Intense intranuclear and intracytoplasmic AIV antigen staining within neurons and neuroglia. Immunohistochemistry. ABC method using anti-NP monoclonal antibody HB65, hematoxylin counterstain. Bar 100 µm.
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pone-0006706-g003: Histopathology and immunohistochemistry of brain from infected ducks.(A) Brain, Cerebrum; Duck at 5 dpc. Congestion shown by hematoxylin-eosin staining. Bar 100 µm. (B) Brain, Cerebrum; Duck at 6 dpc. Intense intranuclear and intracytoplasmic AIV antigen staining within neurons and neuroglia. Immunohistochemistry. ABC method using anti-NP monoclonal antibody HB65, hematoxylin counterstain. Bar 100 µm.

Mentions: The control duck, which died at 6 dpc showed moderate congestion of the liver and edema of the brain. In histopathology, the cerebrum was severely congested, multifocally there was neuropil degeneration with mild vacuolation (Figure 3A) hemorrhage and glial nodules. Ventricles of the cerebrum were filled with blood, and a mild lymphoplasmacellular meningoencephalitis with few macrophages was present. Within the lungs there was a moderate congestion and edema. Besides this, severe heterophilic infiltrates, predominantly adjacent to parabronchi were observed. The heart and the liver showed mild multifocal parenchymal degeneration accompanied by lymphoplasma-histiocytic infiltrates. Influenza virus nucleoprotein was detected by immunohistochemistry within the brain (neurons and glial cells, Figure 3B), the liver (hepatocytes), the lung (bronchiolar epithelium and alveolar macrophages) and the heart (myocardiocytes). One more duck died at 5 dpc with abovementioned clinical signs, but due to loss of its wing tag, it could not be unambiguously assigned to either H4 or control groups (see also footnote 6 in Table 2). Ducks surviving until 24 dpc did not reveal any gross lesions.


Highly pathogenic avian influenza virus infection of mallards with homo- and heterosubtypic immunity induced by low pathogenic avian influenza viruses.

Fereidouni SR, Starick E, Beer M, Wilking H, Kalthoff D, Grund C, Häuslaigner R, Breithaupt A, Lange E, Harder TC - PLoS ONE (2009)

Histopathology and immunohistochemistry of brain from infected ducks.(A) Brain, Cerebrum; Duck at 5 dpc. Congestion shown by hematoxylin-eosin staining. Bar 100 µm. (B) Brain, Cerebrum; Duck at 6 dpc. Intense intranuclear and intracytoplasmic AIV antigen staining within neurons and neuroglia. Immunohistochemistry. ABC method using anti-NP monoclonal antibody HB65, hematoxylin counterstain. Bar 100 µm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2724736&req=5

pone-0006706-g003: Histopathology and immunohistochemistry of brain from infected ducks.(A) Brain, Cerebrum; Duck at 5 dpc. Congestion shown by hematoxylin-eosin staining. Bar 100 µm. (B) Brain, Cerebrum; Duck at 6 dpc. Intense intranuclear and intracytoplasmic AIV antigen staining within neurons and neuroglia. Immunohistochemistry. ABC method using anti-NP monoclonal antibody HB65, hematoxylin counterstain. Bar 100 µm.
Mentions: The control duck, which died at 6 dpc showed moderate congestion of the liver and edema of the brain. In histopathology, the cerebrum was severely congested, multifocally there was neuropil degeneration with mild vacuolation (Figure 3A) hemorrhage and glial nodules. Ventricles of the cerebrum were filled with blood, and a mild lymphoplasmacellular meningoencephalitis with few macrophages was present. Within the lungs there was a moderate congestion and edema. Besides this, severe heterophilic infiltrates, predominantly adjacent to parabronchi were observed. The heart and the liver showed mild multifocal parenchymal degeneration accompanied by lymphoplasma-histiocytic infiltrates. Influenza virus nucleoprotein was detected by immunohistochemistry within the brain (neurons and glial cells, Figure 3B), the liver (hepatocytes), the lung (bronchiolar epithelium and alveolar macrophages) and the heart (myocardiocytes). One more duck died at 5 dpc with abovementioned clinical signs, but due to loss of its wing tag, it could not be unambiguously assigned to either H4 or control groups (see also footnote 6 in Table 2). Ducks surviving until 24 dpc did not reveal any gross lesions.

Bottom Line: The potential role of wild birds as carriers of highly pathogenic avian influenza virus (HPAIV) subtype H5N1 is still a matter of debate.In mallards with homosubtypic immunity induced by LPAIV infection, clinical disease was absent and shedding of HPAIV from respiratory and intestinal tracts was grossly reduced compared to the heterosubtypic and control groups (mean GEC/100 microl at 3 dpi: 3.0 x 10(2) vs. 2.3 x 10(4) vs. 8.7 x 10(4); p<0.05).We conclude that the epidemiology of HPAIV H5N1 in mallards and probably other aquatic wild bird species is massively influenced by interfering immunity induced by prior homo- and heterosubtypic LPAIV infections.

View Article: PubMed Central - PubMed

Affiliation: Friedrich-Loeffler-Institut (FLI), Insel Riems, Germany. sasan.fereidouni@fli.bund.de

ABSTRACT
The potential role of wild birds as carriers of highly pathogenic avian influenza virus (HPAIV) subtype H5N1 is still a matter of debate. Consecutive or simultaneous infections with different subtypes of influenza viruses of low pathogenicity (LPAIV) are very common in wild duck populations. To better understand the epidemiology and pathogenesis of HPAIV H5N1 infections in natural ecosystems, we investigated the influence of prior infection of mallards with homo- (H5N2) and heterosubtypic (H4N6) LPAIV on exposure to HPAIV H5N1. In mallards with homosubtypic immunity induced by LPAIV infection, clinical disease was absent and shedding of HPAIV from respiratory and intestinal tracts was grossly reduced compared to the heterosubtypic and control groups (mean GEC/100 microl at 3 dpi: 3.0 x 10(2) vs. 2.3 x 10(4) vs. 8.7 x 10(4); p<0.05). Heterosubtypic immunity induced by an H4N6 infection mediated a similar but less pronounced effect. We conclude that the epidemiology of HPAIV H5N1 in mallards and probably other aquatic wild bird species is massively influenced by interfering immunity induced by prior homo- and heterosubtypic LPAIV infections.

Show MeSH
Related in: MedlinePlus