Morphological Changes in Bird Viscera in Experimental Infection by Highly Pathogenic H5N1 Avian Influenza Virus

Шестопалова, Л. В.; Shkurupiy, V. A.; Sharkova, T. V.; Шестопалов, А. М.

doi:10.1007/s10517-009-0376-7

Cited by 3 publications

(2 citation statements)

References 12 publications

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“…Although multiple experimental trials have been conducted with low pathogenic avian influenza (LPAI) and HPAI viruses in wild birds, most of these have used mallards ( Anas platyrhynchos domesticus ) and other mallard-type domestic ducks as experimental models [ 3 4 14 21 28 33 ]. However, the results obtained for mallards cannot be extrapolated to all Anseriformes or any Charadriiformes species.…”

Section: Introductionmentioning

confidence: 99%

Experimental infection and pathology of clade 2.2 H5N1 virus in gulls

et al. 2016

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During 2006, H5N1 HPAI caused an epizootic in wild birds, resulting in a die-off of Laridae in the Novosibirsk region at Chany Lake. In the present study, we infected common gulls (Larus canus) with a high dose of the H5N1 HPAI virus isolated from a common gull to determine if severe disease could be induced over the 28 day experimental period. Moderate clinical signs including diarrhea, conjunctivitis, respiratory distress and neurological signs were observed in virus-inoculated birds, and 50% died. The most common microscopic lesions observed were necrosis of the pancreas, mild encephalitis, mild myocarditis, liver parenchymal hemorrhages, lymphocytic hepatitis, parabronchi lumen hemorrhages and interstitial pneumonia. High viral titers were shed from the oropharyngeal route and virus was still detected in one bird at 25 days after infection. In the cloaca, the virus was detected sporadically in lower titers. The virus was transmitted to direct contact gulls. Thus, infected gulls can pose a significant risk of H5N1 HPAIV transmission to other wild migratory waterfowl and pose a risk to more susceptible poultry species. These findings have important implications regarding the mode of transmission and potential risks of H5N1 HPAI spread by gulls.

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Section: Introductionmentioning

confidence: 99%

Experimental infection and pathology of clade 2.2 H5N1 virus in gulls

et al. 2016

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“…It has been shown earlier that macrophages are one of main target cells for influenza A viruses [10][11][12]. Influenza viruses were identified in lung macrophages as early as one day after infection when studying mice lung samples using immunohistochemical analysis based on Inf A antibody against influenza A (H5N1) virus antigen.…”

Section: Study Resultsmentioning

confidence: 99%

Morphofunctional status and the role of mononuclear phagocyte system lung compartment in the pathogenesis of influenza A (H5N1) in mammals

Ковнер¹,

Потапова²,

Shkurupy³

et al. 2013

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Influenza and other respiratory viral infections account for 80%-90% of infectious pathologies. Influenza A (H5N1) virus has an apparent pneumotropism, and therefore the lung compartment of mononuclear phagocyte system plays an important role in antiviral immunity. Lung macrophages are active phagocytes expressing variety of antiviral factors. The investigation of morphofunctional status of lung macrophages and evaluation of their role in mammal antiviral response in a mouse model were performed within the study. Methods: Light microscopy using standard hematoxylin-eosin, and Van-Gizon's picrofuchsin staining. Immunohistochemistry using influenza A antigen marker specific primary antibodies, myeloperoxidase, cathepsin D, lysozyme, NO synthase, pro-inflammatory cytokines, cells of CD68 macrophage lineage, PCNA proliferative activity. Morphometric and statistical analysis. Results: Influenza A virus antigen was detected in lung macrophages starting from day 1 to day 14 of infection which corresponds with the beginning of convalescence and may be suggestive of prolonged persistence of virus. On the one hand, the cytopathic effects of the virus lead to lung macrophages death mainly via apoptosis through activation of caspase cascade, including caspase-3 and caspase-9. On the other hand, the observed activation of PCNA proliferation marker, perhaps, allows to support the pool of lung macrophages not only by their recruitment from bone marrow but also by their proliferation in situ. The increase of mononuclear phagocyte system cells expressing antiviral factors depended on the stage of infection. In the early stage, there was an increase of number of cells expressing lysozyme, myeloperoxidase, cathepsin D, endothelial NO syn-thase (eNOS) followed by the increase of number of macrophages expressing inducible NO synthase (iNOS), pro-inflammatory cytokines and interleukins.

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