Viral-host interaction in kidney reveals strategies to escape host immunity and persistently shed virus to the urine

Ou, Xumin; Mao, Sai; Jiang, Yifan; Zhang, Shengyong; Chen, Ke; Ma, Guangqiang; Cheng, Anchun; Wang, Mingshu; Zhu, Dekang; Chen, Shun; Jia, Renyong; Liu, Mafeng; Sun, Kunfeng; Yang, Qiao; Wu, Ying; Chen, Xiaoyue

doi:10.18632/oncotarget.14227

Cited by 23 publications

(33 citation statements)

References 43 publications

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“…Each section was examined under an optical microscope. IHC was conducted as described previously (Ou et al, 2017). Briefly, slides were boiled in Tris/EDTA pH 9.0 for 20 min.…”

Section: Hematoxylin and Eosin (He) Staining And Immunohistochemistrymentioning

confidence: 99%

Autophagy Is a Potential Therapeutic Target Against Duck Tembusu Virus Infection in vivo

Pan

Cheng

et al. 2020

Front. Cell. Infect. Microbiol.

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Duck tembusu virus (DTMUV) is newly emerged in poultry and causes great losses to the breeding industry in China and neighboring countries. Effective antiviral strategies are still being studied. Autophagy is a cellular degradative pathway, and our lab's previous data show that autophagy promotes DTMUV replication in vitro. To study the role of autophagy further in vivo, we utilized ducks as the animal model to investigate the autophagy responses in DTMUV-targeted tissues. And also, we utilized autophagy regulators, including Rapamycin (Rapa) as the autophagy enhancer, 3-Methyladenine (3-MA) and Chloroquine (CQ) as the autophagy inhibitors, to adjust the host autophagic levels and then study the effects of autophagy on tissue damages and virus replication. As a result, we first found DTMUV infection trigged autophagy and autophagy regulator treatments regulated autophagy levels successfully in duck spleens and brains. Next, we found that autophagy inhibitors inhibited DTMUV replication and alleviated DTMUV-induced pathological symptoms, whereas the autophagy inducer treatment led to the opposite effects. And we also found that autophagic regulation was correlated with the expression of innate immune genes, including pattern recognition receptors, type I interferons, and cytokines, and caused different effects in different tissues. In summary, we demonstrated that autophagy facilitated DTMUV replication, aggravated the developments of pathological symptoms and possibly counteracts the host's innate immunity response in vivo.

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“…Each section was examined under an optical microscope. IHC was conducted as described previously (Ou et al, 2017). Briefly, slides were boiled in Tris/EDTA pH 9.0 for 20 min.…”

Section: Hematoxylin and Eosin (He) Staining And Immunohistochemistrymentioning

confidence: 99%

Autophagy Is a Potential Therapeutic Target Against Duck Tembusu Virus Infection in vivo

Pan

Cheng

et al. 2020

Front. Cell. Infect. Microbiol.

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“…Infection of adult ducks with DHAV-1 was previously shown to result in transient cytokine storms in their kidneys 14 . However, only one study has investigated virus-host interactions in the livers of DHAV-1-infected ducklings.…”

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confidence: 99%

Cytokine storms are primarily responsible for the rapid death of ducklings infected with duck hepatitis A virus type 1

Xie

Wang

Cheng

et al. 2018

Sci Rep

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Duck hepatitis A virus type 1 (DHAV-1) is one of the most harmful pathogens in the duck industry. The infection of adult ducks with DHAV-1 was previously shown to result in transient cytokine storms in their kidneys. To understand how DHAV-1 infection impacts the host liver, we conducted animal experiments with the virulent CH DHAV-1 strain and the attenuated CH60 commercial vaccine strain. Visual observation and standard hematoxylin and eosin staining were performed to detect pathological damage in the liver, and viral copy numbers and cytokine expression in the liver were evaluated by quantitative PCR. The CH strain (108.4 copies/mg) had higher viral titers than the CH60 strain (104.9 copies/mg) in the liver and caused ecchymotic hemorrhaging on the liver surface. Additionally, livers from ducklings inoculated with the CH strain were significantly infiltrated by numerous red blood cells, accompanied by severe cytokine storms, but similar signs were not observed in the livers of ducklings inoculated with the CH60 strain. In conclusion, the severe cytokine storm caused by the CH strain apparently induces hemorrhagic lesions in the liver, which might be a key factor in the rapid death of ducklings.

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“…In this study, the interferons (IFN-α/β/γ) and interleukins (IL-1β/2/4/6) were highly up-regulated from 2-dpi to 6-dpi (Figure 4A ). Interestingly, the period of cytokine storms was similar to that in kidney infected with DHAV-1 [ 33 ]. Simultaneously, viral copies in liver were decreased under the course of cytokine storms (Figure 4A ).…”

Section: Resultsmentioning

confidence: 97%

The neglected avian hepatotropic virus induces acute and chronic hepatitis in ducks: an alternative model for hepatology

Mao

Cao

et al. 2017

Oncotarget

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Duck Hepatitis A Virus (DHAV) belongs to the Avihepatovirus, which is also classified into Picornaviridae with Hepatovirus, Hepatitis A Virus (HAV). In humans, the pathogenesis of HAV is not well understood because of limited work with animal models. Here, we investigated the progress of duck viral hepatitis caused by DHAV and their potential for dissecting the pathogenesis of HAV. During the course of infection, the duck model had undergone hepatocellular lesions (vacuolation, acidophilic degeneration and steatosis), lymphocytes recruitment (neutrophil granulocytes, heterophilic granulocytes and T cells or plasm cells) and repair (activation of hepatic stellate cells, fibrosis and regeneration). Coincident with liver injury, the serum biomarkers, aspartate aminotransferase and alanine transaminase were significantly increased. Moreover, comparatively lower CD4+ and CD8+ T-cells were recruited to the liver, which might lead to a persistent infection (40 wk). Because DHAV and HAV have similar genomic structure, biological phenotypes and can easily replicate in liver. And half of fibrosis-related genes had high homology between humans and ducks. Considering these similarity in pathological and virological phenotypes, we proposed that the ducks might be an alternatively small animal model that would provide insight into the pathogenesis of viral hepatitis, fibrosis and liver regeneration.

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Viral-host interaction in kidney reveals strategies to escape host immunity and persistently shed virus to the urine

Cited by 23 publications

References 43 publications

Autophagy Is a Potential Therapeutic Target Against Duck Tembusu Virus Infection in vivo

Autophagy Is a Potential Therapeutic Target Against Duck Tembusu Virus Infection in vivo

Cytokine storms are primarily responsible for the rapid death of ducklings infected with duck hepatitis A virus type 1

The neglected avian hepatotropic virus induces acute and chronic hepatitis in ducks: an alternative model for hepatology

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