Single-chain intracellular antibodies inhibit influenza virus replication by disrupting interaction of proteins involved in viral replication and transcription

Mukhtar, Muhammad Mahmood; Li, Shengfeng; Li, Wei; Wan, Ting; Mu, Yongxin; Wei, Wei; Liu, Kang; Rasool, Sahibzada Tasleem; Xiao, Yibei; Zhu, Ying; Wu, Jianguo

doi:10.1016/j.biocel.2008.07.001

Cited by 32 publications

(33 citation statements)

References 34 publications

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“…Influenza virus strain A/chicken/Hubei/327/2004 (H5N1) was used as described previously (1,21). Two other influenza virus strains used in this study, A/Yamagata/120/86 (H1N1) and A/Hong Kong/498/97 (H3N2), were provided by the China Center Type Culture Collection.…”

Section: Virus and Cell Culturementioning

confidence: 99%

“…The viral titers were measured 48 h or at indicated time points postinfection with a hemagglutination assay in U-shaped 96-well plates, as described previously (21). Total RNA extraction, reverse transcription, and real-time PCR were conducted to detect the relative RNA levels of nucleoprotein (NP)-mRNA, NP-cRNA, and NP-viral RNA (vRNA), as described previously (21).…”

Section: Measurement Of Influenza Virus Replicationmentioning

confidence: 99%

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IL-32: A Host Proinflammatory Factor against Influenza Viral Replication Is Upregulated by Aberrant Epigenetic Modifications during Influenza A Virus Infection

Sun

Liu

et al. 2010

The Journal of Immunology

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106

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Section: Virus and Cell Culturementioning

confidence: 99%

Section: Measurement Of Influenza Virus Replicationmentioning

confidence: 99%

IL-32: A Host Proinflammatory Factor against Influenza Viral Replication Is Upregulated by Aberrant Epigenetic Modifications during Influenza A Virus Infection

Sun

Liu

et al. 2010

The Journal of Immunology

Self Cite

114

106

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“…IV strain A/chicken/Hubei/327/2004 (H5N1) was used as described previously [1,9]. Human Embryonic Kidney cells (HEK 293T) were cultured in DMEM, human lung epithelial cells (A549) were cultured in F12K medium, human T-cell lymphoblast-like cells (Jurkat) and human leukemic monocyte lymphoma cells (U937) were cultured in RPMI 1640 medium.…”

Section: Virus and Cell Culturementioning

confidence: 99%

Negative feedback regulation of IL‐32 production by iNOS activation in response to dsRNA or influenza virus infection

Yang

Liu

et al. 2009

Eur J Immunol

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iNOS plays an important role in mediating inflammation. In this study, we found that iNOSderived NO was increased 2.4-fold in the serum samples of 101 patients infected with influenza A virus in comparison with samples of 105 healthy individuals. In A549 human lung epithelial cells, infection with influenza A virus or stimulation with poly(I:C)1IFN-c resulted in increased mRNA and protein levels of both IL-32 and iNOS, with subsequent release of NO. Overexpression of IL-32 resulted in upregulated iNOS expression with subsequent NO production. Knock down of IL-32 by IL-32-specific siRNA resulted in the inhibition of dsRNA-induced expression of iNOS and NO release, indicating that IL-32 is an upstream regulatory factor of dsRNA-triggered iNOS production. Surprisingly, over-expression of iNOS resulted in the reduction of IL-32 expression, and suppression of iNOS by the selective iNOS inhibitor S-methylisothiourea sulfate stimulated IL-32 expression, indicating that a negative feedback mechanism operates between the iNOS/NO and IL-32 systems. These findings suggest that influenza A virus infection activates IL-32 and iNOS expression by a heretofore unrecognized complex mechanism, in which the two pro-inflammatory factors regulate each other, involving positive and negative feedback regulatory loops.Key words: Gene regulation . IL-32 . Inducible nitric oxide synthase . Inflammation . Influenza virus IntroductionIn a recent study we found that influenza virus (IV) infection in patients is associated with increased serum levels of the inflammatory cytokine IL-32 and the COX-2-induced prostaglandin PGE 2 . In vitro, IV infection of A549 lung epithelial cells resulted in release of IL-32 and activation of COX-2 expression [1]. As a proxy of virus infection we used stimulation of the cells with dsRNA1IFN-g, a combination previously shown to act synergistically when administered intratracheally [2] and in mouse peritoneal macrophages in vitro [3]. We demonstrated that production of IL-32 depends on prior COX-2 activation, but also that IL-32 can exert negative feedback control over activation of .In the present study we have pursued the analysis of these inflammatory pathways by testing for activation of the iNOS gene and subsequent production of NO. NO is synthesized from L-arginine by NOS in numerous mammalian cells and tissues and plays a critical role in signal modulation during immune responses, chronic inflammation and carcinogenesis. Three isoforms of NOS have been identified until now: two constitutively expressed and calciumdependent isoforms endothelial NOS and neuronal NOS; one inducible and calcium-independent isoform (iNOS), which catalyzes the production of high amount of NO in response to diverse stimuli [4].Increased IL-32 and iNOS expression stimulated by viral infections has been reported in previous investigations [1,5,6]. However, the function of IL-32 in the pro-inflammatory network is still unclear. Since IL-32 and iNOS are obligatory mediators of inflammation, the Fig. 1D) expression levels in cell ...

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“…It is possible that secretory IgA can react with the newly synthesized protein in the infected epithelial cells, thus affecting the replication and assembly of the virus, promoting recovery from infection. 5,[19][20][21] These results indicated that NP as a candidate antigen of UIV immunized intranasally can effectively induce mucosal and cell-mediated immunity to provide protection against new emerging influenza viruses infection. Therefore, mucosal immunization might be more effective than other parenteral routes of immunization for clearing the virus, which might be due to the fact that recruitment of immune cells to the infection site in mice immunized intranasally occurred more quickly than in mice immunized parenterally.…”

Section: Discussionmentioning

confidence: 83%

Cross-protection against influenza virus infection by intranasal administration of nucleoprotein-based vaccine with compound 48/80 adjuvant

Zheng

Liu

Shen

et al. 2015

Human Vaccines & Immunotherapeutics

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Single-chain intracellular antibodies inhibit influenza virus replication by disrupting interaction of proteins involved in viral replication and transcription

Cited by 32 publications

References 34 publications

IL-32: A Host Proinflammatory Factor against Influenza Viral Replication Is Upregulated by Aberrant Epigenetic Modifications during Influenza A Virus Infection

IL-32: A Host Proinflammatory Factor against Influenza Viral Replication Is Upregulated by Aberrant Epigenetic Modifications during Influenza A Virus Infection

Negative feedback regulation of IL‐32 production by iNOS activation in response to dsRNA or influenza virus infection

Cross-protection against influenza virus infection by intranasal administration of nucleoprotein-based vaccine with compound 48/80 adjuvant

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