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Background <p>Bovine herpesvirus type 1 (BHV-1) is the primary pathogen responsible for infectious rhinotracheitis in cattle, leading to significant economic losses in the cattle industry. Long non-coding RNAs (lncRNAs) are multifunctional transcriptional regulators that play a role in the regulation of host-virus-specific interactions.</p> Methods <p>MDBK cells were infected with BHV-1, and the function of lncRNA-MSTRG.16919.1 was evaluated using siRNA-mediated knockdown, as well as lentivirus-mediated stable overexpression of TAK1 and TAB2, respectively. Subsequent analyses were performed via qPCR, Western blotting, and viral titration assays, with the interaction between lncRNA-MSTRG.16919.1 and TAK1 further validated by RNA immunoprecipitation (RIP) assay.</p> Results <p>Our previous study found that lncRNA-MSTRG.16919.1 is highly expressed in BHV-1 infected MDBK cells. Functional assays showed that its silencing reduced viral DNA replication, downregulated transcription and protein expression of glycoproteins gB and gD, and decreased virion production, indicating that it promotes BHV-1 proliferation. Further investigation revealed that knockdown of this lncRNA reduced protein levels of TAB1, TAB2, TAB3, and TAK1. RNA immunoprecipitation (RIP) assay demonstrated that endogenous lncRNA-MSTRG.16919.1 physically interacts with the TAK1 protein, particularly during BHV-1 infection. To validate the involvement of the TAK1/TABs complex, we overexpressed TAK1 or TAB2 in cells with lncRNA knockdown. Overexpression restored viral DNA synthesis, gB and gD expression, and virus titers, counteracting the suppression caused by lncRNA silencing. Moreover, TAK1 or TAB2 overexpression elevated protein levels of TAB3, TAB1, TAK1, NF-κB, and JNK.</p> Conclusions <p>These results demonstrate that lncRNA-MSTRG.16919.1 facilitates BHV-1 replication by modulating the TAK1-TABs complex and suggesting the potential involvement of the NF-κB pathway. These findings provide foundational insights for studying the function and regulatory mechanisms of lncRNA-MSTRG.16919.1 in organisms, and contribute to the understanding of the pathogenic mechanisms of BHV-1, aiding in the prevention and control of bovine respiratory diseases.</p>

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LncRNA-MSTRG.16919.1 regulates the proliferation of BHV-1 in MDBK cells through TAK1/TAB1/TAB2/TAB3 complexes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月10日

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  • Fan Zhang,
  • Cai-na Song,
  • Jin-zhu Ma,
  • Li-quan Yu,
  • Chen Peng,
  • Wen-xue Wu,
  • Bai-fen Song

摘要

Background

Bovine herpesvirus type 1 (BHV-1) is the primary pathogen responsible for infectious rhinotracheitis in cattle, leading to significant economic losses in the cattle industry. Long non-coding RNAs (lncRNAs) are multifunctional transcriptional regulators that play a role in the regulation of host-virus-specific interactions.

Methods

MDBK cells were infected with BHV-1, and the function of lncRNA-MSTRG.16919.1 was evaluated using siRNA-mediated knockdown, as well as lentivirus-mediated stable overexpression of TAK1 and TAB2, respectively. Subsequent analyses were performed via qPCR, Western blotting, and viral titration assays, with the interaction between lncRNA-MSTRG.16919.1 and TAK1 further validated by RNA immunoprecipitation (RIP) assay.

Results

Our previous study found that lncRNA-MSTRG.16919.1 is highly expressed in BHV-1 infected MDBK cells. Functional assays showed that its silencing reduced viral DNA replication, downregulated transcription and protein expression of glycoproteins gB and gD, and decreased virion production, indicating that it promotes BHV-1 proliferation. Further investigation revealed that knockdown of this lncRNA reduced protein levels of TAB1, TAB2, TAB3, and TAK1. RNA immunoprecipitation (RIP) assay demonstrated that endogenous lncRNA-MSTRG.16919.1 physically interacts with the TAK1 protein, particularly during BHV-1 infection. To validate the involvement of the TAK1/TABs complex, we overexpressed TAK1 or TAB2 in cells with lncRNA knockdown. Overexpression restored viral DNA synthesis, gB and gD expression, and virus titers, counteracting the suppression caused by lncRNA silencing. Moreover, TAK1 or TAB2 overexpression elevated protein levels of TAB3, TAB1, TAK1, NF-κB, and JNK.

Conclusions

These results demonstrate that lncRNA-MSTRG.16919.1 facilitates BHV-1 replication by modulating the TAK1-TABs complex and suggesting the potential involvement of the NF-κB pathway. These findings provide foundational insights for studying the function and regulatory mechanisms of lncRNA-MSTRG.16919.1 in organisms, and contribute to the understanding of the pathogenic mechanisms of BHV-1, aiding in the prevention and control of bovine respiratory diseases.