Rab18 binds to classical swine fever virus NS5A and mediates viral replication and assembly in swine umbilical vein endothelial cells

Zhang, Liang; Zhao, Di; Jin, Mingxing; Song, Mengzhao; Liu, Shanchuan; Guo, Kangkang; Zhang, Yanming

doi:10.1080/21505594.2020.1767356

Cited by 17 publications

(12 citation statements)

References 50 publications

(76 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These host proteins could be divided into the following categories according to their possible mechanism involved in CSFV replication. (1) Many members of the small Rab GTPase family, such as Rab1A [58], Rab1b [59], Rab2 [60], Rab5 [61,62], Rab7, Rab11 [62], Rab18 [63], and Rab25 [64], play a critical role in CSFV replication. For example, Rab18 interacts with CSFV NS5A and mediates viral RNA replication and virion assembly [63].…”

Section: Host Proteins Whose Function Defect Exert Anti-csfv Effectsmentioning

confidence: 99%

“…(1) Many members of the small Rab GTPase family, such as Rab1A [58], Rab1b [59], Rab2 [60], Rab5 [61,62], Rab7, Rab11 [62], Rab18 [63], and Rab25 [64], play a critical role in CSFV replication. For example, Rab18 interacts with CSFV NS5A and mediates viral RNA replication and virion assembly [63]. (2) Some proteins could promote CSFV replication possibly through regulating the level of interferons (IFNs), such as PKR [65], PCBP1 [66], and MERTK [67].…”

Section: Host Proteins Whose Function Defect Exert Anti-csfv Effectsmentioning

confidence: 99%

See 1 more Smart Citation

Anti-Classical Swine Fever Virus Strategies

et al. 2021

View full text Add to dashboard Cite

Classical swine fever (CSF), caused by CSF virus (CSFV), is a highly contagious swine disease with high morbidity and mortality, which has caused significant economic losses to the pig industry worldwide. Biosecurity measures and vaccination are the main methods for prevention and control of CSF since no specific drug is available for the effective treatment of CSF. Although a series of biosecurity and vaccination strategies have been developed to curb the outbreak events, it is still difficult to eliminate CSF in CSF-endemic and re-emerging areas. Thus, in addition to implementing enhanced biosecurity measures and exploring more effective CSF vaccines, other strategies are also needed for effectively controlling CSF. Currently, more and more research about anti-CSFV strategies was carried out by scientists, because of the great prospects and value of anti-CSFV strategies in the prevention and control of CSF. Additionally, studies on anti-CSFV strategies could be used as a reference for other viruses in the Flaviviridae family, such as hepatitis C virus, dengue virus, and Zika virus. In this review, we aim to summarize the research on anti-CSFV strategies. In detail, host proteins affecting CSFV replication, drug candidates with anti-CSFV effects, and RNA interference (RNAi) targeting CSFV viral genes were mentioned and the possible mechanisms related to anti-CSFV effects were also summarized.

show abstract

Section: Host Proteins Whose Function Defect Exert Anti-csfv Effectsmentioning

confidence: 99%

Section: Host Proteins Whose Function Defect Exert Anti-csfv Effectsmentioning

confidence: 99%

Anti-Classical Swine Fever Virus Strategies

et al. 2021

View full text Add to dashboard Cite

show abstract

“…GST-pull down assays. GST pull-down assays were carried out as previously described (34). Briefly, the pGEX-GST-MMP-9 plasmid was transformed into BL21 cells to GST-MMP-9 proteins.…”

Section: Co-immunoprecipitation (Co-ip) Assays Myc-integrin β1mentioning

confidence: 99%

Downregulation of miR‑29b‑3p promotes α‑tubulin deacetylation by targeting the interaction of matrix metalloproteinase‑9 with integrin β1 in nasal polyps

Liu

et al. 2021

Int J Mol Med

View full text Add to dashboard Cite

Matrix metalloproteinase (MMP)-9 is a key enzyme responsible for extracellular matrix degradation and contributes to the progressive histological changes observed in lower respiratory tract infections. Integrin β1 and α-tubulin are potential MMP-9-interacting proteins, and microRNA (miR)-29b-3p can regulate MMP-9 expression. MMP-9 is highly expressed in chronic rhinosinusitis with nasal polyps (cRSwNPs), regardless of its effects on miR-29b-3p, integrin β1 and α-tubulin expression. In the present study, samples from 100 patients with cRSwNPs were examined via reverse transcription-quantitative PcR to assess the mRNA expression of miR-29b-3p, and western blotting was performed to assess the protein expression of MMP-2, MMP-9, acetyl-α-tubulin, integrin β1 and tissue inhibitor of metalloproteinase 1 (TIMP-1). A dual-luciferase reporter assay was used to verify the direct binding of miR-29b-3p and MMP-2/MMP-9. co-immunoprecipitation (co-IP) and GST pull-down assays showed that integrin β1 and α-tubulin were MMP-9-interacting proteins. Cell viability, apoptosis and inflammatory cytokine levels were determined via a Cell Counting Kit-8 assay, flow cytometry and ELISA, respectively. miR-29b-3p expression was found to be positively correlated with MMP-2 and MMP-9 expression. Whereas, TIMP-1 expression was negatively correlated with MMP-2 and MMP-9 expression. The dual-luciferase assay revealed that miR-29b-3p targeted the 3' untranslated region of MMP-2/MMP-9. The co-IP and GST pull-down assays showed that MMP-9 could directly bind to integrin β1 and indirectly bind to α-tubulin. Finally, the overexpression of miR-29b-3p decreased the expression of MMP-9 and increased the levels of acetyl-α-tubulin. By contrast, the knockdown of miR-29b-3p increased the expression of MMP-9 and decreased the levels of acetyl-α-tubulin. Additionally, MMP-9 expression was found to be negatively correlated with acetyl-α-tubulin expression. Of note, the expression of integrin β1 did not change following the overexpression and knockdown of MMP-9. Finally, the overexpression of miR-29b-3p not only decreased MMP-9 expression, but also alleviated lipopolysaccharide-induced inflammation in NP69 cells. The results showed that the downregulation of miR-29b-3p promoted α-tubulin deacetylation by increasing the number of MMP-9-integrin β1 complexes in cRSwNPs, thus targeting miR-29b-3p/MMP-9 may be a potential novel strategy for the clinical treatment of cRSwNPs.

show abstract

“…For instance, BVDV NS5A protein similarly localizes to LDs, but it is not known to which LDs-associated protein it specifically binds (Isken et al, 2014). Recent studies show that the LDs-associated proteins Rab18 and Rab1A interact with CSFV NS5A protein, an essential replicase component, which have been shown to mediate viral replication and assembly process (Lin et al, 2018;Zhang et al, 2020). Additionally, Rab5, which also belongs to the family of small GTPases, enhances CSFV proliferation and interacts with the viral NS4B protein to promote the formation of NS4B associated complexes (Lin et al, 2017).…”

Section: Lds-involvement In Flaviviridae Life Cyclementioning

confidence: 99%

Molecular Events Occurring in Lipophagy and Its Regulation in Flaviviridae Infection

Fan

Zou

et al. 2021

Front. Microbiol.

View full text Add to dashboard Cite

Diseases caused by Flaviviridae have a wide global and economic impact due to high morbidity and mortality. Flaviviridae infection usually leads to severe, acute or chronic diseases, such as liver injury and liver cancer resulting from hepatitis C virus (HCV) infection, dengue hemorrhagic fever (DHF) or dengue shock syndrome (DSS) caused by dengue virus (DENV). Given the highly complex pathogenesis of Flaviviridae infections, they are still not fully understood at present. Accumulating evidence suggests that host autophagy is disrupted to regulate the life cycle of Flaviviridae. Organelle-specific autophagy is able to selectively target different organelles for quality control, which is essential for regulating cellular homeostasis. As an important sub process of autophagy, lipophagy regulates lipid metabolism by targeting lipid droplets (LDs) and is also closely related to the infection of a variety of pathogenic microorganisms. In this review, we briefly understand the LDs interaction relationship with Flaviviridae infection, outline the molecular events of how lipophagy occurs and the related research progress on the regulatory mechanisms of lipophagy in Flaviviridae infection. Exploring the crosstalk between viral infection and lipophagy induced molecular events may provide new avenues for antiviral therapy.

show abstract

Rab18 binds to classical swine fever virus NS5A and mediates viral replication and assembly in swine umbilical vein endothelial cells

Cited by 17 publications

References 50 publications

Anti-Classical Swine Fever Virus Strategies

Anti-Classical Swine Fever Virus Strategies

Downregulation of miR‑29b‑3p promotes α‑tubulin deacetylation by targeting the interaction of matrix metalloproteinase‑9 with integrin β1 in nasal polyps

Molecular Events Occurring in Lipophagy and Its Regulation in Flaviviridae Infection

Contact Info

Product

Resources

About