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

Sharkova, T. V.; Потапова, О. В.; Shkurupy, V. A.; Shestopalov, А. М.; Drozdov, Ignat; Шестопалова, Л. В.

doi:10.1007/s10517-008-0262-8

Cited by 5 publications

(2 citation statements)

References 6 publications

(6 reference statements)

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“…Some studies have shown that IAVs of many subtypes (H1N1, H5N1, and H7N9) not only cause lung infection but also impair multiple extrapulmonary tissues and organs, such as the brain, heart, thymus, pancreas, liver, spleen, adrenal glands, kidneys, ovaries, and fallopian tubes. The resulting diseases and disorders include encephalitis, myopericarditis, thymus atrophy, pancreatitis, diabetes, subtotal destructive changes in the liver, spleen atrophy, and acute kidney damage 3‐9 . Certain components of IAVs, such as the NP antigen and RNA, were also found in these organs 9,10 …”

Section: Introductionmentioning

confidence: 99%

Immunodepression induced by influenza A virus (H1N1) in lymphoid organs functions as a pathogenic mechanism

Zhang

et al. 2020

Clin Exp Pharma Physio

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In recent years, the frequency of influenza epidemics around the world has posed a great threat to the lives of people, especially those in developing countries. However, it is unclear which organs are the targets of influenza A viruses (IAVs) and what histopathology is caused by IAVs. In this study, BALB/c female mice were infected with H1N1 by nasal inoculation for 5 days. After euthanasia, the brain, heart, lungs, thymus, liver, spleen, hilar lymph nodes, pancreas, kidneys, and adrenal glands were collected. Among these organs, only the lungs, thymus, spleen, and hilar lymph nodes showed lesions. Lung histopathology was characterized by widening of the septum, lymphocyte infiltration, alveolar effusion, and alveolar hyaline membrane formation. The thymus and spleen exhibited atrophy due to the apoptosis of numerous lymphocytes. Although the hilar lymph nodes were enlarged, lymphocyte apoptosis still occurred. The nucleocapsid protein (NP) of IAVs was present not only in the lungs but also in the thymus, spleen, and hilar lymph nodes. In peripheral blood, CD19+B lymphocyte levels clearly decreased whileCD3+CD8+T and CD3+CD4+T lymphocyte levels temporarily decreased but subsequently increased. These results demonstrate that H1N1 in the lungs could reach lymphoid organs, induce the depletion of B and T lymphocytes in peripheral blood and lymphoid organs, and suppress adaptive immunity.

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Section: Introductionmentioning

confidence: 99%

Immunodepression induced by influenza A virus (H1N1) in lymphoid organs functions as a pathogenic mechanism

Zhang

et al. 2020

Clin Exp Pharma Physio

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“…This dysregulation makes a significant contribution to the high mortality of H5N1 influenza(Cheung et al, 2002 ; de Jong et al, 2006 ; Us, 2008 ; Cillóniz et al, 2009 ; Tisoncik et al, 2012 ). In addition to the respiratory systems, IAV infection can also affect other organs of the digestive and nervous systems including the spleen, liver, small intestine and brain(Leon'teva et al, 1989 ; Sharkova et al, 2008 ; Chaves et al, 2014 ; Zhang et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

H5N1 Influenza a Virus Replicates Productively in Pancreatic Cells and Induces Apoptosis and Pro-Inflammatory Cytokine Response

Huo

Xiao

Zhang

et al. 2018

Front. Cell. Infect. Microbiol.

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The inflammatory response and apoptosis have been proved to have a crucial role in the pathogenesis of the influenza A virus (IAV). Previous studies indicated that while IAV commonly causes pancreatitis and pancreatic damage in naturally and experimentally infected animals, the molecular mechanisms of the pathogenesis of IAV infection are less reported. In the present study, we showed for the first time that both avian-like (α-2,3-linked) and human-like (α-2,6-linked) sialic acid (SA) receptors were expressed by the mouse pancreatic cancer cell line PAN02 and the human pancreatic cancer cell line PANC-1. Using growth kinetics experiments, we also showed that PAN02 and PANC-1 cells supported the productive replication of the H5N1 highly pathogenic avian influenza while exhibited the limited replication of IAV subtypes H1N1 and H7N2 in vitro. The in vivo infection of H5N1 in pancreatic cells was confirmed by the histopathological and immunohistochemical staining of pancreas tissue from mice. Other than H1N1 and H7N2, severe damage and extensive positive signals were observed in pancreas of H5N1 infected mice. All three virus subtypes induced apoptosis but also triggered the infected PAN02 and PANC-1 cells to release pro-inflammatory cytokines and chemokines including interferon (IFN)-α, IFN-β, IFN-γ, chemokine (C-C motif) ligand 2 (CCL2), tumor necrosis factor (TNF)-α, and interleukin (IL)-6. Notably, the subtypes of H5N1 could significantly upregulate these cytokines and chemokines in both two cells when compared with H1N1 and H7N2. The present data provide further understanding of the pathogenesis of H5N1 IAV in pancreatic cells derived from humans and mammals and may also benefit the development of new treatment against H5N1 influenza virus infection.

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インフルエンザA（H3N2）感染あるいはその治療薬投与を契機に発症した非昏睡型急性肝不全の1例(A case of acute hepatic failure without coma due to influenza virus A (H3N2) infection or treatment)

裕章¹,

覚²,

貴弘³

et al. 2020

Nihon Kyukyu Igakukai Zasshi: Japanese Journal of Japanese Asso

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要旨症例は54歳の女性，当院受診2日前より全身倦怠感を認め，インフルエンザAと診断され，バロキサビルマルボキシル，ツムラ麻黄湯，アセトアミノフェンを内服処方され経過をみていた。その後，自宅で動けなくなり救急搬送となり，非昏睡型急性肝不全，急性腎障害と診断した。与芝の劇症化予測式（Z=2.677）陽性のため，劇症化の可能性が高いと判断し，血漿交換，持続血液濾過透析を施行した。その後，肝逸脱酵素は急速に改善し，第28病日に退院した。飲酒歴はなく，各種ウイルスマーカー，自己免疫性肝炎の自己抗体は陰性であった。また，DDW–J–2004薬剤性肝障害ワークショップのスコアリングでは8点と薬物性肝障害を強く疑ったが，被疑薬と考えたバロキサビルマルボキシル，ツムラ麻黄湯，アセトアミノフェンのリンパ球刺激試験は陰性であった。急性肝不全の原因は不明だが，インフルエンザウイルス感染による急性肝不全の報告例は非常に稀であること，バロキサビルマルボキシルによる急性肝不全の副作用報告もないことから，貴重な症例と考え，今回報告した。

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

Cited by 5 publications

References 6 publications

Immunodepression induced by influenza A virus (H1N1) in lymphoid organs functions as a pathogenic mechanism

Immunodepression induced by influenza A virus (H1N1) in lymphoid organs functions as a pathogenic mechanism

H5N1 Influenza a Virus Replicates Productively in Pancreatic Cells and Induces Apoptosis and Pro-Inflammatory Cytokine Response

インフルエンザA（H3N2）感染あるいはその治療薬投与を契機に発症した非昏睡型急性肝不全の1例(A case of acute hepatic failure without coma due to influenza virus A (H3N2) infection or treatment)

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