Porcine Circovirus-Like Virus P1 Inhibits Wnt Signaling Pathway in Vivo and in Vitro

Zhu, Xun; Li, Wen; Sheng, Shaoyang; Wang, Wei; Xiao, Qin; Qu, Meng; Hu, Yue; Liu, Chuanmin; He, Kongwang

doi:10.3389/fmicb.2018.00390

Cited by 12 publications

(9 citation statements)

References 31 publications

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“…Multiple studies have shown that different virus may employ different mechanisms to manipulate the process of Wnt/β-catenin pathway's participation in viral replication [20,21,31]. In this study, β-catenin up-regulated the expression of IFN-β and ISG, inhibited BPIV3 proliferation.…”

Section: Discussionmentioning

confidence: 59%

“…Many other viral infections have been shown to correlate with the functionality of β-catenin. For example, both Porcine Circovirus-like virus and Human Cytomegalovirus inhibit the classical Wnt signal pathway post-infection [8,31]. When Wnt/β-catenin pathway is at the deactivation stage, the protein kinase GSK3β phosphorylates serine at site 33 and 37 on β-catenin [17].…”

Section: Discussionmentioning

confidence: 99%

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Beta-catenin inhibits bovine parainfluenza virus type 3 replication via innate immunity pathway

et al. 2020

BMC Vet Res

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Background: Bovine parainfluenza virus type 3 (BPIV3) is one of the important viral respiratory agents associated with the bovine respiratory disease complex (BRDC) in cattle. Previous study has demonstrated that infection of BPIV3 causes innate immune response within the host cell. β-catenin is a key component of the Wnt/β-catenin signal pathway which is involved in the regulation of interferon-beta (IFN-β) transcription. Some viruses can activate while others can inhibit the Wnt/β-catenin signaling pathway. However, the role of β-catenin in BPIV3 infection remains unclear.Results: Here we found that the expression of β-catenin mRNA was up-regulated and β-catenin protein was downregulated after BPIV3 infection in MDBK cells. Moreover, it was confirmed that overexpression of β-catenin suppressed BPIV3 replication and knockdown of β-catenin promoted viral replication, suggesting that β-catenin inhibits BPIV3 replication. Furthermore, IFN-β signal pathway and virus titer analysis using the GSK3β inhibitor (LiCl) revealed that Wnt/β-catenin can serve as a mechanism to suppress virus replication in infected cells. The results indicated that LiCl promoted the expression and accumulation in the nucleus of β-catenin, which further promoted the expression of IFN-β and OSA1 and suppressed BPIV3 replication. Most importantly, BPIV3 down-regulating βcatenin protein expression was due to degradation of GSK3β mediated proteasome pathway. Conclusions: In summary, we discovered the relationship between β-catenin and BPIV3 replication. These results provided further insight into the study of BPIV3 pathogenesis.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Beta-catenin inhibits bovine parainfluenza virus type 3 replication via innate immunity pathway

et al. 2020

BMC Vet Res

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“…Some viruses can activate or deactivate the Wnt/β-catenin pathway. These include viruses such as HIV [ 31 ], porcine circovirus-like virus P1 [ 21 ], HCMV [ 32 ], and HCV [ 17 ]. On the other hand, the Wnt/β-catenin signaling pathway has varying effects on different viruses.…”

Section: Discussionmentioning

confidence: 99%

“…Several reports have demonstrated the interaction of the Wnt/β-catenin signaling pathway with human and animal viruses, including human immunodeficiency virus (HIV) [ 14 ], herpes simplex virus 1 (HSV1) [ 15 ], hepatitis B virus (HBV) [ 16 ], hepatitis C virus (HCV) [ 17 ], influenza virus (IAV) [ 18 ], porcine reproductive and respiratory syndrome virus (PRRSV) [ 19 , 20 ], porcine circovirus-like virus P1 [ 21 ], bovine parainfluenza virus type 3 [ 22 ], and bovine herpesvirus 1 [ 23 ]. Some of these viruses activate the Wnt/β-catenin signaling pathway, while others deactivate it through diverse mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Regulation of Avian Leukosis Virus Subgroup J Replication by Wnt/β-Catenin Signaling Pathway

Qiao

Cheng

et al. 2021

Viruses

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Wnt/β-catenin signaling is a highly conserved pathway related to a variety of biological processes in different cells. The regulation of replication of various viruses by Wnt/β-catenin signaling pathway has been reported. However, the interaction between the Wnt/β-catenin pathway and avian leukosis virus is unknown. In the present study, we investigated the effect of modulating the Wnt/β-catenin pathway during avian leukosis virus subgroup J (ALV-J) infection. The activation of the Wnt/β-catenin pathway by GSK-3 inhibitor increased ALV-J mRNA, viral protein expression, and virus production in CEF cells. This increase was suppressed by iCRT14, one of the specific inhibitors of the Wnt/β-catenin signaling pathway. Moreover, treatment with iCRT14 reduced virus titer and viral gene expression significantly in CEF and LMH cells in a dose-dependent manner. Inhibition Wnt/β-catenin signaling pathway by knockdown of β-catenin reduced virus proliferation in CEF cells also. Collectively, these results suggested that the status of Wnt/β-catenin signaling pathway modulated ALV-J replication. These studies extend our understanding of the role of Wnt/β-catenin signaling pathway in ALV-J replication and make a new contribution to understanding the virus–host interactions of avian leukosis virus.

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“…Little is known about the cellular events caused by infection with P1 virus. The study showed that several porcine genes, such as MMP2, were down-regulated not only in tissues of infected pigs and mice but also in ST cells and that the virus induces the Wnt signaling pathways [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

Interaction of porcine circovirus-like virus P1 capsid protein with host proteins

Zhu

Zhang

et al. 2021

BMC Vet Res

Self Cite

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Background Porcine circovirus-like virus P1 is a relatively new kind of virus that is closely related to the post-weaning multisystemic wasting syndrome, congenital tremors, and abortions in swine. The molecular mechanisms of P1 virus infection and pathogenesis are fully unknown. To analyze P1 and its host interactions, we used a yeast two-hybrid (Y2H) assay to identify cellular proteins interacting with the Cap of the P1 virus. In this study, the Cap of the P1 virus exhibited no self-activation and toxicity to yeast cells and was used as bait to screen the Y2H library prepared from the pancreas tissue. Results Five cellular proteins (EEP, Ral GDS, Bcl-2-L-12, CPS1, and one not identified) were found to interact with P1 Cap. The interaction between Cap and Ral GDS was confirmed by co-immunoprecipitation. Conclusions Our data are likely to support the future investigation of the underlying mechanism of P1 infection and pathogenesis.

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Porcine Circovirus-Like Virus P1 Inhibits Wnt Signaling Pathway in Vivo and in Vitro

Cited by 12 publications

References 31 publications

Beta-catenin inhibits bovine parainfluenza virus type 3 replication via innate immunity pathway

Beta-catenin inhibits bovine parainfluenza virus type 3 replication via innate immunity pathway

Regulation of Avian Leukosis Virus Subgroup J Replication by Wnt/β-Catenin Signaling Pathway

Interaction of porcine circovirus-like virus P1 capsid protein with host proteins

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