Characterization of the gene expression profile of human bocavirus

Chen, Aaron Yun; Cheng, Fang; Lou, Sai; Luo, Yong; Liu, Zhengwen; Delwart, Eric; Pintel, David J.; Qiu, Jianming

doi:10.1016/j.virol.2010.04.014

Cited by 112 publications

(166 citation statements)

References 60 publications

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“…A previous report (53) and the results of this study (Fig. 6B, 6C) showed that NP1 mostly located in the nucleus.…”

Section: Hbov Np1 Interacts With Irf-3supporting

confidence: 83%

“…Although the overexpression of NP1 and NS1 significantly inhibited IFN-b production, research on the HBoV gene-expression profile showed that NP1 was much more abundant than was NS1 (53). Therefore, we focused on NP1 in the following experiment.…”

Section: Hbov Np1 Inhibits Both Sev-and Poly(da-dt)-stimulated Ifn-b mentioning

confidence: 99%

“…A recent study of its geneexpression profiles showed that HBoV generally possesses similar genetic information as do bovine parvovirus and canine minute virus (53,54). In addition to two structural proteins, VP1 and VP2, HBoV encodes three nonstructural proteins: NS1-70, NS1, and NP1.…”

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confidence: 99%

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Human Bocavirus NP1 Inhibits IFN-β Production by Blocking Association of IFN Regulatory Factor 3 with IFNB Promoter

Zhang

Zheng

Luo

et al. 2012

The Journal of Immunology

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Human bocavirus (HBoV) mainly infects young children. Although many infected children suffer from respiratory or gastroenteric tract diseases, an association between HBoV and these diseases is not definite. Because modulation of type I IFN is crucial for viruses to establish efficient replication, in this study, we tested whether HBoV modulates type I IFN production. We observed that a nearly full-length HBoV clone significantly reduced both Sendai virus (SeV)- and poly(deoxyadenylic-thymidylic) acid-induced IFN-β production. Further study showed that NP1 blocked IFN-β activation in response to SeV, poly(deoxyadenylic-thymidylic) acid, and IFN-β pathway inducers, including retinoic acid-inducible protein I, mitochondrial antiviral signaling protein, inhibitor of κB kinase ε, and TANK-binding kinase 1. In addition, NP1 interfered with IRF-3–responsive PRD(III-I) promoter activated by SeV and a constitutively active mutant of IRF-3 (IRF-3/5D). Although NP1 suppressed the IRF-3 pathway, it did not affect IRF-3 activation processes, including phosphorylation, dimerization, and nuclear translocation. Coimmunoprecipitation assays confirmed the interaction between NP1 and IRF-3. Additional deletion mutagenesis and coimmunoprecipitation assays revealed that NP1 bound to the DNA-binding domain of IRF-3, resulting in the interruption of an association between IRF-3 and IFNB promoter. Altogether, our results indicate that HBoV NP1 blocks IFN production through a unique mechanism. To our knowledge, this is the first study to investigate the modulation of innate immunity by HBoV. Our findings suggest a potential immune-evasion mechanism used by HBoV and provide a basis for better understanding HBoV pathogenesis.

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“…A previous report (53) and the results of this study (Fig. 6B, 6C) showed that NP1 mostly located in the nucleus.…”

Section: Hbov Np1 Interacts With Irf-3supporting

confidence: 83%

Section: Hbov Np1 Inhibits Both Sev-and Poly(da-dt)-stimulated Ifn-b mentioning

confidence: 99%

See 1 more Smart Citation

Human Bocavirus NP1 Inhibits IFN-β Production by Blocking Association of IFN Regulatory Factor 3 with IFNB Promoter

Zhang

Zheng

Luo

et al. 2012

The Journal of Immunology

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“…In a previous report, human airway epithelia infected with HBoV were revealed to result in cilia loss and airway epithelial cell hypertrophy; however this was not associated with apoptotic or necrotic cell death (23). Similarly, a previous study demonstrated that HBoV nonstructural protein failed to cause cell death (5). However, in the present study, we demonstrated that HBoV recombination expressing vector (pWHL-1) induced proliferation inhibition, apoptosis and autophagy in HBECs.…”

Section: Discussionsupporting

confidence: 46%

“…HBoV encodes three nonstructural proteins including: NP1, NS1 and NS1-70, in addition to two structural proteins, VP1 and VP2. HBoV NP1 is a nuclear protein, which has an important role in the DNA replication process of HBoV within the nuclei of infected cells (5,6). It has been reported that NP1 is able to cause cell cycle arrest at G2/M phase followed by apoptosis, via the mitochondrion pathway in HeLa cells (7).…”

Section: Introductionmentioning

confidence: 99%

Human bocavirus induces apoptosis and autophagy in human bronchial epithelial cells

Deng

Liu

Yang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. Human bocavirus (HBoV) is classified in the Bocavirus genus within the Parvoviridae family, first identified from children with respiratory diseases. Previous studies have investigated the stimulating effect of HBoV on cell apoptosis and autophagy. In the present study, human bronchial epithelial cells (HBECs) were utilized to examine the mechanism of HBoV recombination expressing vector (pWHL-1) on the promotion of cell apoptosis and autophagy. The results from the present study indicated that pWHL-1 inhibited the proliferation of HBECs in a time-dependent manner. Additionally, pWHL-1induced apoptosis, as substantiated by an increased apoptotic rate and presence of autophagosomes. Following pWHL-1 transfection, proliferating cell nuclear antigen, caspase-3 and B cell lymphoma 2 (Bcl-2) protein expression levels were decreased, with the exception of Bcl-2 associated x (Bax) protein, which increased. mRNA and protein expression levels of microtubule-associated protein 1A/1B-light chain 3 (LC3) II and autophagy protein 5 were increased in pWHL-1-transfected HBECs, whereas, the mRNA and protein levels of LC3I and sequestosome 1 were decreased. Notably, pWHL-1 also enhanced the activation of p53 and inhibited AKT activation in HBECs. Results from the present study suggest that pWHL-1 induces apoptosis and autophagy, thus providing a novel insight into the effect of HBoV and its uses in respiratory diseases.

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Parvovirus B19V, Bocaviruses, and Other Human Parvoviruses

Söderlund‐Venermo

2023

ClinMicroNow

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Parvoviruses are small, nonenveloped icosahedral viruses with a linear single‐stranded‐DNA (ssDNA) genome in the family Parvoviridae in the realm Monodnaviria . The family Parvoviridae is divided into three subfamilies, Parvovirinae , Densovirinae , and the new Hamaparvovirinae , on the basis of their ability to infect vertebrates, invertebrates, or both, respectively, and their NS1 amino acid sequences. The first human parvoviruses identified were the nonpathogenic adeno‐associated viruses of the genus Dependoparvovirus , which are increasingly used in gene therapy. Human bocavirus (HBoV1) has the typical structure of a member of the Parvoviridae . The most common test for diagnosis of HBoV1 infection is DNA detection by qualitative PCR. Parvoviruses are unable to induce cells to divide, so they require actively dividing cells for their replication.

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Characterization of the gene expression profile of human bocavirus

Cited by 112 publications

References 60 publications

Human Bocavirus NP1 Inhibits IFN-β Production by Blocking Association of IFN Regulatory Factor 3 with IFNB Promoter

Human Bocavirus NP1 Inhibits IFN-β Production by Blocking Association of IFN Regulatory Factor 3 with IFNB Promoter

Human bocavirus induces apoptosis and autophagy in human bronchial epithelial cells

Parvovirus B19V, Bocaviruses, and Other Human Parvoviruses

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