Pathogenesis of Infectious Disease of Mice Caused by H5N1 Avian Influenza Virus

Evseenko, V. A.; Sharshov, Kirill; Bukin, Eugenij; Zaykovskaya, А. V.; Ternovoy, V. A.; Ignatyev, G. M.; Shestopalov, А. М.; Нетесов, С. В.; Shkurupiy, V. A.; Drozdov, I. G.

doi:10.1007/s10517-009-0375-8

Cited by 4 publications

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References 6 publications

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“…Neuromorphogenesis of viral infection was studied in series II on A/goose/Krasnoozerskoye/627/05 strain, characterized by the highest neurotropism, high pathogenic activity, and causing generalized infection with mortality reaching 85% in experimental animals [1][2][3].…”

Section: Resultsmentioning

confidence: 99%

Structural Changes in the Brain of Mice Infected with Influenza A/H5N1 Virus

et al. 2009

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Structural changes in the brain of outbred mice were studied after infection with influenza A/H5N1 strain isolated in the Novosibirsk region. High mortality was observed after intranasal infection. Examination of brain specimens revealed vasculopathies with thrombosis of the microcirculatory vessels, pericellular and perivascular edema with multifocal ischemic necrosis, hyperplasia of glial cells, caspase-dependent apoptosis of neurons caused by the cytopathic effect of the virus, and hypercytokinemia.

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Section: Resultsmentioning

confidence: 99%

Structural Changes in the Brain of Mice Infected with Influenza A/H5N1 Virus

et al. 2009

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“…These changes are probably associated with dysregulation in production of proinflammatory and antiinflammatory cytokines by the mononuclear phagocyte system and natural killer cells. Previous studies showed that the concentration of proinflammatory cytokines interleukin-6 (IL-6) and TNF-α increases, while the content of IFN-γ decreases in mammalian blood plasma during the early period after infection [2]. Cytokine-inactivated sinusoidal cells synthesize eicosanoids (thromboxanes, prostacyclins, etc.…”

Section: Resultsmentioning

confidence: 99%

“…These changes are probably associated with increased secretion of proinflammatory cytokines IL-10 and IL-2 [2] and alternative activation of macrophages, which results in the decrease in cytotoxic properties, high-intensity endocytosis of cell destruction products [3], and simultaneous elevation of reparative activity of hepatocytes. …”

Section: Resultsmentioning

confidence: 99%

Structural changes in the liver of mice infected with avian influenza virus subtype H5N1

et al. 2008

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Intranasal infection of male outbred rats with isolate of influenza A virus subtype H5N1 (A/Gs/Krasnoozerskoye/627/05) from the Novosibirsk region was followed by high mortality of experimental animals. Morphological study of liver samples revealed subtotal destructive changes in the liver parenchyma (proteinosis and centrolobular necroses), which was related to hemodynamic disorders and cytokine dysregulation. The decrease in reparative activity of hepatocytes was probably followed by hepatocellular failure and contributed to high mortality rate from this infection (up to 85%).

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“…Because these cells are reported to play essential roles in the control of influenza virus [14], IFN-γ is also thought to be associated with the pathogenesis of influenza [3,10]. For example, H5N1 HPAIV was found to induce IFN-γ in mammals [4], and early administration of exogenous IFN-γ during influenza virus infection stimulates NK cell proliferation and function in infected lungs [24]. An HPAIV A/ Vietnam/1203/2003 (H5N1) was also found to induce IFN-γ in the lung and spleen of chickens [11].…”

Section: Discussionmentioning

confidence: 99%

The Pathogenicity and Host Immune Response Associated with H5N1 Highly Pathogenic Avian Influenza Virus in Quail

Uno

Usui

Soda

et al. 2013

The Journal of Veterinary Medical Science

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ABSTRACT. Quail, like chickens, are susceptible to H5N1 subtype highly pathogenic avian influenza virus (HPAIV). Both birds experience high mortality, but quail usually survive a few more days than chicken. To understand why, we monitored quail and chickens after inoculation with 10 6 fifty-percent egg infectious doses of HPAIV A/whooper swan/Aomori/1/2008 (H5N1). The clinical course initiated as depression at 48 hr post inoculation (h.p.i.) in quail and at 36 h.p.i. in chicken, and all infected birds died. Mean death time of quail (91 hr) was significantly longer than that of chicken (66 hr). The virus titers of most tissue samples collected before death were not significantly different. At 24 h.p.i., interferon gamma (IFN-γ) mRNA expression in peripheral blood mononuclear cells (PBMC) was up-regulated in the quail but down-regulated in the chicken, although TLR-7 and seven other cytokines showed no significant differences between quail and chicken. The viral load in quail PBMC was significantly lower than that in chickens. These results suggest that the induction of IFN-γ after HPAIV infection in quail is related to lower titer of HPAIV. In conclusion, the different clinical courses observed between quail and chicken infected with H5N1 HPAIV might be caused by different IFN-γ responses against the HPAIV infection.

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Pathogenesis of Infectious Disease of Mice Caused by H5N1 Avian Influenza Virus

Abstract: The pathogenesis of a disease caused by Qinghai-like H5N1 influenza virus in BALB/c mice was studied. Clinical, morphological, and immunological characteristics of the experimental infection caused by highly pathogenic A/duck/Tuva/01/06/ (H5N1) virus are described.

Cited by 4 publications

References 6 publications

Structural Changes in the Brain of Mice Infected with Influenza A/H5N1 Virus

Structural Changes in the Brain of Mice Infected with Influenza A/H5N1 Virus

Structural changes in the liver of mice infected with avian influenza virus subtype H5N1

The Pathogenicity and Host Immune Response Associated with H5N1 Highly Pathogenic Avian Influenza Virus in Quail

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