Interplay between CTHRC1 and the SU protein of avian leukosis virus subgroup J (ALV-J) facilitates viral replication

Pang, Yi-Hsin; Zhou, Defang; Xue, Jingwen; Zhou, Jing; Zhang, Ya; Zheng, Gaoying; Yuan, Shiyu; Yao, Yongxiu; Cheng, Ziqiang

doi:10.1016/j.virusres.2019.02.014

Cited by 11 publications

(11 citation statements)

References 37 publications

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“…As shown in Figure 2B, CTHRC1 was mainly located in the cytoplasm and was activated in the blood lymphocytes of ALV-J infected chickens than those of normal chickens. CTHRC1 was interacted with ALV-J SU protein and co-localized in the cytoplasm (23), which was in line with our results obtained in Figure 2B that CTHRC1 and ALV-J were co-located in the cytoplasm of lymphocytes. Meanwhile, according to Cui et al (1999), ALV-J was not infected with erythrocytes of blood, which only transport ALV-J, but it can infect lymphocytes of blood (32).…”

Section: Collagen Triple Helix Repeat Containing-1 Is Activated In Blsupporting

confidence: 92%

“…Thus far, the studies of CTHRC1 focus on the field of oncology; there is rare coverage on the role of CTHRC1 in the field of viral replication. Recently, we have firstly reported that CTHRC1 facilitates ALV-J replication through interaction with the SU protein of ALV-J, which indicates that CTHRC1 plays a crucial role in regulating ALV-J replication (23). These studies may provide new enlightenment to the study of interaction between host protein(s) and ALV-J, and these expand the biological function of CTHRC1 in the field of virus replication (23).…”

Section: Introductionmentioning

confidence: 89%

“…ALV-J strain GM0209 was isolated from a broiler breeder maintained in our laboratory (7). Monoclonal antibody directed against ALV-J SU protein was produced as described previously (23,24). Rabbit polyclonal antibody against CTHRC1 was purchased from Absin Corporation (Shanghai, China).…”

Section: Virus Antibodies and Experimental Animalsmentioning

confidence: 99%

“…Recently, we have firstly reported that CTHRC1 facilitates ALV-J replication through interaction with the SU protein of ALV-J, which indicates that CTHRC1 plays a crucial role in regulating ALV-J replication (23). These studies may provide new enlightenment to the study of interaction between host protein(s) and ALV-J, and these expand the biological function of CTHRC1 in the field of virus replication (23). However, the distribution and expression of CTHRC1 in chicken tissues upon ALV-J infection are still unknown, which may provide a theoretical basis for the subsequent research of ALV-J and CTHRC1.…”

Section: Introductionmentioning

confidence: 99%

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The Distribution and Localization of Collagen Triple Helix Repeat Containing-1 in Naturally and Experimentally Avian Leukosis Virus Subgroup J-Infected Chickens

Pang

Zhou

et al. 2020

Front. Vet. Sci.

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Collagen triple helix repeat containing-1 (CTHRC1) has recently been identified as avian leukosis virus subgroup J (ALV-J) replication-dependent factor that remarkably facilitates ALV-J replication via interaction with the envelope glycoprotein (SU) of ALV-J. However, the dynamic distribution and localization of CTHRC1 in various tissues upon ALV-J infection are still unknown. In this study, data revealed that the levels of CTHRC1 were significantly increased in various tissues and that the protein was mainly located in the cytoplasm and nucleus of parenchymal cells in tissues of chickens that were infected by ALV-J naturally and experimentally. Interestingly, CTHRC1 was also observed in leukocytes other than erythrocytes in congested veins of ALV-J-infected tissues. Consequently, the positive cells in these veins were confirmed as lymphocytes by laser confocal microscopy. Taken together, these results conclude that the CTHRC1 is an inducible protein and exhibited ubiquitous expression in ALV-J-infected chickens, which may provide basic information for in-depth study of ALV-J infection and replication mechanisms.

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Section: Collagen Triple Helix Repeat Containing-1 Is Activated In Blsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 89%

Section: Virus Antibodies and Experimental Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Distribution and Localization of Collagen Triple Helix Repeat Containing-1 in Naturally and Experimentally Avian Leukosis Virus Subgroup J-Infected Chickens

Pang

Zhou

et al. 2020

Front. Vet. Sci.

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“…In order to screen differentially expressed proteins that plays a key role in cell signal transduction under ALV-J infection,protein lysates from ALV-J-infected CEF and normal CEF were collected for proteomic analysis and bioinformatics analysis. The experimental process, iTRAQ labelled LC-MS/MS, and bioinformatics analysis were all followed as our previous description [48].…”

Section: Proteomics Assay and Bioinformatics Analysismentioning

confidence: 99%

Lyn inhibited BCR signal pathway mediates B-cell anergy induced by avian leukosis virus subgroup J

Zheng

Yang

et al. 2020

Preprint

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Background: Immune tolerance induced by retrovirus is a prerequisite for tumorigeness. We had reported that B-cell anergy was the main reason for immune tolerance induced by avian leukosis virus subgroup J (ALV-J). However, the molecular mechanism remains unclear. Results: Initially, we found that Lyn showed down-regulation in chick embryo fibroblasts (CEF) and up-regulation in B-cells infected by ALV-J. So, we speculated that tyrosine kinase Lyn plays a key role in B-cell anergy induced by ALV-J. Confocal laser scanning microscopy (CLSM) and co-immunoprecipitation (Co-IP) results demonstrated that ALV-J indirectly regulated the expression of Lyn. To further investigate the role and regulatory mechanism of Lyn in B-cell anergy induced by ALV-J, the expression levels of Lyn and Syk at different phosphorylation site, the Ca 2+ mobilization, and the expression levels of NF-κB p65 protein in vitro and vivo were detected in B-cells. The result showed that Ca 2+ mobilization was delayed and p65 expression level was decreased in B-cells after ALV-J infection. Consistently, the retrieve of Ca 2+ mobilization, expression levels of NF-κB p65 were found after RNA interference of Lyn. Subsequently, we demonstrated that the activation of phosphorylated Lyn protein at Tyr507 site played a critical role in B-cells anergy, which were verified by the fact of the significantly up-regulation of the expression levels of phosphorylated Syk protein at Tyr525/526 site when RNA interference for Lyn were performed in B-cells. Furthermore, immunohistochemical (IHC) staining results confirmed that the expression levels of Lyn phosphorylated protein at Tyr507 site in bursal cells were increased, while the expression levels of Syk phosphorylated protein at Tyr525/526 sites were decreased. Conclusions: These findings suggested that Lyn inhibited BCR signal pathway mediates B-cell anergy under ALV-J infection，which will provide a new insight for revealing the molecular mechanism of immune tolerance induced by ALV-J. Keywords: avian leukosis virus subgroup J , B-cell anergy, immune tolerance, Lyn, Syk

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Chicken interferon regulatory factor 7 (IRF7) can control ALV-J virus infection by triggering type I interferon production through affecting genes related with innate immune signaling pathway

Wang

Yang

Yin

et al. 2021

Developmental & Comparative Immunology

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Interplay between CTHRC1 and the SU protein of avian leukosis virus subgroup J (ALV-J) facilitates viral replication

Cited by 11 publications

References 37 publications

The Distribution and Localization of Collagen Triple Helix Repeat Containing-1 in Naturally and Experimentally Avian Leukosis Virus Subgroup J-Infected Chickens

The Distribution and Localization of Collagen Triple Helix Repeat Containing-1 in Naturally and Experimentally Avian Leukosis Virus Subgroup J-Infected Chickens

Lyn inhibited BCR signal pathway mediates B-cell anergy induced by avian leukosis virus subgroup J

Chicken interferon regulatory factor 7 (IRF7) can control ALV-J virus infection by triggering type I interferon production through affecting genes related with innate immune signaling pathway

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