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      Establishment of a stable CHO cell line with high level expression of recombinant porcine IFN-β

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          Abstract

          A CHO cell clone (CHO-PoIFN-β) with stable porcine IFN-β expression under control of CMV promoter was selected under G418 pressure. In a 25 cm 2 cell culture flask (5 ml culture medium), the cumulative protein yield of recombinant PoIFN-β reached 2.3 × 10 6 IU/ml. This cells clone maintained stable expression for at least 20 generations even in the absence of G418 selection pressure. The expressed recombinant PoIFN-β could induce the expression of porcine Mx protein in PK15 cells, and activate the chicken Mx promoter-controlled luciferase reporter gene expression, confirming that the recombinant PoIFN-β has the biological activity of natural porcine type-I interferon. In addition, the recombinant PoIFN-β fully protected PK15 cells against 1000 TCID 50 of porcine transmissible gastroenteritis virus and pseudo-rabies virus infection, demonstrating its high potential in therapeutic applications. This is the first report of establishing a mammalian cell line with stable expression of porcine IFN-β.

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          Classical swine fever virus Npro interacts with interferon regulatory factor 3 and induces its proteasomal degradation.

          Artur Summerfield, Yoshihiro Sakoda, Jon-Duri Tratschin … (2007)
          Viruses have evolved a multitude of strategies to subvert the innate immune system by interfering with components of the alpha/beta interferon (IFN-alpha/beta) induction and signaling pathway. It is well established that the pestiviruses prevent IFN-alpha/beta induction in their primary target cells, such as epitheloidal and endothelial cells, macrophages, and conventional dendritic cells, a phenotype mediated by the viral protein N(pro). Central players in the IFN-alpha/beta induction cascade are interferon regulatory factor 3 (IRF3) and IRF7. Recently, it was proposed that classical swine fever virus (CSFV), the porcine pestivirus, induced the loss of IRF3 by inhibiting the transcription of IRF3 mRNA. In the present study, we show that endogenous IRF3 and IRF3 expressed from a cytomegalovirus (CMV) promoter are depleted in the presence of CSFV by means of N(pro), while CSFV does not inhibit CMV promoter-driven protein expression. We also demonstrate that CSFV does not reduce the transcriptional activity of the IRF3 promoter and does not affect the stability of IRF3 mRNA. In fact, CSFV N(pro) induces proteasomal degradation of IRF3, as demonstrated by proteasome inhibition studies. Furthermore, N(pro) coprecipitates with IRF3, suggesting that the proteasomal degradation of IRF3 is induced by a direct or indirect interaction with N(pro). Finally, we show that N(pro) does not downregulate IRF7 expression.
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            In vivo and in vitro interferon (IFN) studies with the porcine reproductive and respiratory syndrome virus (PRRSV).

            K Van Reeth, M Pensaert, W Buddaert (1997)
            Some of the interactions between the porcine reproductive and respiratory syndrome virus (PRRSV) and the porcine interferon-alpha (IFN-alpha) system were studied. In a first experiment, it was shown that pretreatment of primary porcine alveolar macrophages (AMs) with recombinant porcine (rPo) IFN-alpha 1 resulted in significant reductions of PRRSV yield and numbers of antigen expressing cells. In a second experiment, sensitivity of PRRSV to IFN-alpha was confirmed in vivo. In pigs inoculated with porcine respiratory coronavirus (PRCV)--a potent inducer of endogenous IFN-alpha in the lungs of pigs--followed 2 days later by PRRSV--lung PRRSV titers were 1.7 to 2.9 log10 TCID50 reduced compared to those in singly PRRSV inoculated pigs. It was concluded therefore that PRRSV has a fairly good sensitivity to the antiviral effects of IFN-alpha. A third experiment documented that in vivo PRRSV infection generally does not affect PRCV-induced IFN-alpha production in the lungs of pigs. In addition, it was shown that the IFN-inducing capacity of PRRSV is at least 159 times lower than that of PRCV. This finding suggests that cells other than AMs may be responsible for IFN production in the lungs of pigs.
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              Inverse interference: how viruses fight the interferon system.

              Friedemann Weber, Georg Kochs, Otto Haller (2004)
              Viruses need to multiply extensively in the infected host in order to ensure transmission to new hosts and survival as a population. This is a formidable task, given the powerful innate and adaptive immune responses of the host. In particular, the interferon (IFN) system plays an important role in limiting virus spread at an early stage of infection. It has become increasingly clear that viruses have evolved multiple strategies to escape the IFN system. They either inhibit IFN synthesis, bind and inactivate secreted IFN molecules, block IFN-activated signaling, or disturb the action of IFN-induced antiviral proteins. The molecular mechanisms involved range from a broad shut-off of the host cell metabolism to fine-tuned elimination of key components of the IFN system. Type I (alpha/beta) IFNs are produced in direct response to virus infection and double-stranded RNA (dsRNA) molecules that are sensed as a danger signal by infected cells. IFNs induce the expression of a number of antiviral proteins, some of which are again activated by dsRNA. Therefore, many viruses produce dsRNA-binding proteins to sequester the danger signal or express virulence genes that target specific components of the IFN system, such as members of the IFN regulatory factor (IRF) family or components of the JAK-STAT signaling pathway. Finally, some viruses have adopted means to directly suppress the very antiviral effector proteins of the IFN-induced antiviral state directed against them. Evidently, viruses and their host's innate immune responses have coevolved, leading to a subtle balance between virus-promoting and virus-inhibiting factors. A better understanding of virus-host interactions is now emerging with great implications for vaccine development and drug design.
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                Author and article information

                Contributors
                Kehe Huang
                Zhigao Bu
                Journal
                Journal ID (nlm-ta): Cytokine
                Journal ID (iso-abbrev): Cytokine
                Title: Cytokine
                Publisher: Published by Elsevier Ltd.
                ISSN (Print): 1043-4666
                ISSN (Electronic): 1096-0023
                Publication date PMC-release: 1 April 2011
                Publication date (Print): June 2011
                Publication date (Electronic): 1 April 2011
                Volume: 54
                Issue: 3
                Pages: 324-329
                Affiliations
                [a ]National Key Laboratory of Veterinary Biotechnology, Harbin Veterinary Research Institute, Chinese Academy of Agricultural Sciences (CAAS), 427 Maduan Street, Harbin 150001, People’s Republic of China
                [b ]College of Veterinary Medicine, Nanjing Agricultural University, No. 1 Weigang, Nanjing 210095, People’s Republic of China
                Author notes
                [* ]Corresponding authors. Tel.: +86 451 85935062; fax: +86 451 82733132 (Z. Bu), tel.: +86 25 84395507; fax: +86 25 84398669 (K. Huang). khhuang@ 123456njau.edu.cn zgb@ 123456hvri.ac.cn
                Article
                Publisher ID: S1043-4666(10)00773-8
                DOI: 10.1016/j.cyto.2010.12.002
                PMC ID: 7128424
                PubMed ID: 21459017
                SO-VID: a38f0a96-5ec5-42c2-9642-2552f4df30ae
                Copyright statement: Copyright © 2010 Published by Elsevier Ltd.
                License:

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                Date received : 28 March 2010
                Date revision received : 26 June 2010
                Date accepted : 2 December 2010
                Categories
                Subject: Article

                ScienceOpen disciplines: Cell biology
                Keywords: porcine interferon-β,cho-k1 cells,stable expression,biological activity,antiviral activity
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: porcine interferon-β, cho-k1 cells, stable expression, biological activity, antiviral activity

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