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      Novel goose-origin astrovirus infection in geese: the effect of age at infection

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          Abstract

          Since 2017, a serious infectious disease characterized by visceral gout has emerged in China's main goose-producing regions. The disease has caused huge economic losses to China's goose industry. In our previous study, we determined that the pathogen causing gout in goslings is a novel goose-origin astrovirus, designated as AStV/SDPY/Goose/1116/17 (AStV-SDPY) strain. To investigate the effect of host age on the outcome of novel goose-origin astrovirus infection, 200 1-day-old healthy goslings were selected to be experimentally infected at 1, 5, 15, 25, and 35 D of age. It was shown in experimental infection that the AStV-SDPY strain was highly pathogenic in goslings aged 1 to 15 D, causing growth repression, severe visceral urate deposition, and even death, whereas goslings infected at 25 and 35 D of age showed mild symptoms. Histopathologic examination indicated that lesions occurred mainly in the kidney and liver of infected goslings, which is correlated to the severity of clinical signs and gross lesions. Viral RNA was detected in all representative tissues, and virus shedding was detected continuously within 15 D after inoculation. Higher viral copy number, especially in vital organs such as the liver and kidney, was developed in the goslings infected at 1 to 15 D of age than older geese. In addition, clinical chemistry and inflammatory cytokines showed that younger geese are more sensitive to AStV infection. Overall, our study demonstrates that the pathogenicity of AStV-SDPY in goslings is partly associated with the age of infection, laying a foundation for further study of the pathogenic mechanism of this virus.

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          Most cited references36

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          A SIMPLE METHOD OF ESTIMATING FIFTY PER CENT ENDPOINTS12

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            IL-6 pathway in the liver: From physiopathology to therapy.

            Interleukin 6 (IL-6) is a pleiotropic four-helix-bundle cytokine that exerts multiple functions in the body. In the liver, IL-6 is an important inducer of the acute phase response and infection defense. IL-6 is furthermore crucial for hepatocyte homeostasis and is a potent hepatocyte mitogen. It is not only implicated in liver regeneration, but also in metabolic function of the liver. However, persistent activation of the IL-6 signaling pathway is detrimental to the liver and might ultimately result in the development of liver tumors. On target cells IL-6 can bind to the signal transducing subunit gp130 either in complex with the membrane-bound or with the soluble IL-6 receptor to induce intracellular signaling. In this review we describe how these different pathways are involved in the physiology and pathophyiology of the liver. We furthermore discuss how IL-6 pathways can be selectively inhibited and therapeutically exploited for the treatment of liver pathologies.
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              Propionibacterium acnes induces intervertebral disc degeneration by promoting nucleus pulposus cell apoptosis via the TLR2/JNK/mitochondrial-mediated pathway

              Evidence suggests that intervertebral disc degeneration (IVDD) can be induced by Propionibacterium acnes (P. acnes), although the underlying mechanisms are unclear. In this study, we analyzed the pathological changes in degenerated human intervertebral discs (IVDs) infected with P. acnes. Compared with P. acnes-negative samples, P. acnes-positive IVDs showed increased apoptosis of nucleus pulposus cells (NPCs) concomitant with severe IVDD. Then, a P. acnes-inoculated IVD animal model was established, and severe IVDD was induced by P. acnes infection by promoting NPC apoptosis. The results suggested that P. acnes-induced apoptosis of NPCs via the Toll-like receptor 2 (TLR2)/c-Jun N-terminal kinase (JNK) pathway and mitochondrial-mediated cell death. In addition, P. acnes was found to activate autophagy, which likely plays a role in apoptosis of NPCs. Overall, these findings further validated the involvement of P. acnes in the pathology of IVDD and provided evidence that P. acnes-induced apoptosis of NPCs via the TLR2/JNK pathway is likely responsible for the pathology of IVDD.
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                Author and article information

                Contributors
                Journal
                Poult Sci
                Poult Sci
                Poultry Science
                Elsevier
                0032-5791
                1525-3171
                26 June 2020
                September 2020
                26 June 2020
                : 99
                : 9
                : 4323-4333
                Affiliations
                []College of Animal Science and Technology, Shandong Agricultural University, Tai'an, Shandong 271018, China
                []Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, Tai'an, Shandong 271018, China
                []Shandong Provincial Engineering Technology Research Center of Animal Disease Control and Prevention, Shandong Agricultural University, Tai'an, Shandong 271018, China
                Author notes
                Article
                S0032-5791(20)30351-5
                10.1016/j.psj.2020.05.041
                7598121
                32867976
                786d0afa-91cf-4cbf-97fb-4f4b0487cc55
                © 2020 Published by Elsevier Inc. on behalf of Poultry Science Association Inc.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 14 March 2020
                : 22 May 2020
                Categories
                Immunology, Health and Disease

                novel goose-origin astrovirus,goose,viral load,histopathology,age

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