An unconventional BST-2 function: Down-regulation of transient protein expression

Narkpuk, Jaraspim; Wanitchang, Asawin; Kramyu, Jarin; Frantz, Phanramphoei Namprachan; Jongkaewwattana, Anan; Teeravechyan, Samaporn

doi:10.1016/j.bbrc.2014.07.022

Cited by 9 publications

(9 citation statements)

References 40 publications

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“…Multiple studies report that BST-2 inhibits the release of influenza virus-like particles but not infectious viruses (Bruce et al, 2012; Watanabe et al, 2011; Winkler et al, 2012; Yondola et al, 2011). In contrast, other studies found that BST-2 reduces the amount of wild-type viral particles released from infected cells (Mangeat et al, 2012; Narkpuk et al, 2014). Both of these studies used IAV generated through reverse genetics, which may account for the contrasting findings with the studies that saw no effect of BST-2 on release of infectious virus.…”

Section: Resultsmentioning

confidence: 69%

Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus

et al. 2015

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Infection of type II alveolar epithelial (ATII) cells by influenza A viruses (IAV) correlates with severe respiratory disease in humans and mice. To understand pathogenic mechanisms during IAV infection of ATII cells, murine ATII cells were cultured to maintain a differentiated phenotype, infected with IAV-PR8, which causes severe lung pathology in mice, and proteomics analyses were performed using liquid chromatography-mass spectrometry. PR8 infection increased levels of proteins involved in interferon signaling, antigen presentation, and cytoskeleton regulation. Proteins involved in mitochondrial membrane permeability, energy metabolism, and chromatin formation had reduced levels in PR8-infected cells. Phenotypic markers of ATII cells in vivo were identified, confirming the differentiation status of the cultures. Surfactant protein B had decreased levels in PR8-infected cells, which was confirmed by immunoblotting and immunofluorescence assays. Analysis of ATII cell protein profiles will elucidate cellular processes in IAV pathogenesis, which may provide insight into potential therapies to modulate disease severity.

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Section: Resultsmentioning

confidence: 69%

Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus

et al. 2015

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“…PA protein levels roughly corresponded to their effect on BST-2 levels; H4N6 and H6N1 had the greatest amounts of PA protein, followed by the highly pathogenic H5N1 and the pandemic H1N1. PR8 and H3N2 PA levels were notably lower, likely due to the presence of BST-2 itself, which has been previously shown to decrease expression of co-transfected genes (Narkpuk et al, 2014). Indeed, in the absence of BST-2, PA of PR8 and the H3N2 and H5N1 viruses were expressed at higher levels, whereas H4N6 and H6N1 PA were expressed at lower levels (Fig.…”

Section: The Pa Segment Encodes a Common Bst-2 Antagonist In Avian Inmentioning

confidence: 65%

“…To study the impact of BST-2 on human and avian influenza viruses, we first generated an MDCK cell line stably expressing human BST-2 cloned from HeLa cells (Narkpuk et al, 2014) ( Supplementary Fig. 1).…”

Section: Generation Of Bst-2-expressing Cell Linesmentioning

confidence: 99%

“…The human BST-2 coding sequence was amplified from pHW-BST-2 (Narkpuk et al, 2014) with primers carrying the BamHI and NotI restriction sites for cloning into the lentiviral vector pSIN-CSGW-UbEm (a gift from Dr. Yasuhiro Ikeda, Mayo Clinic, Minnesota, USA). HEK293T cells were transfected with the lentiviral vector along with VSV-G-expressing pMD-G (Naldini et al, 1996) and the packaging plasmid pCMV-ΔR8.91 (Zufferey et al, 1997), and supernatants containing lentiviral particles were harvested 48 h post-transfection.…”

Section: Generation Of Cell Lines Stably Expressing Bst-2mentioning

confidence: 99%

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The avian influenza virus PA segment mediates strain-specific antagonism of BST-2/tetherin

2018

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“…Since inhibition of viral transcription or translation is another level of anti‐viral action that leads to inhibition of virus release, it is possible that BST‐2 acts as an anti‐viral factor on multiple levels, inhibiting not only viral release but also viral production. In support of this idea, a recent paper by Narkpuk et al () is interesting, as those authors also reported that BST‐2 expression can down‐regulate viral proteins. Defining the precise action point of BST‐2 in the production of viral proteins will provide valuable information for anti‐viral countermeasures.…”

Section: Discussionmentioning

confidence: 84%

Enhanced production of enveloped viruses in BST‐2‐deficient cell lines

Giao

et al. 2017

Biotech & Bioengineering

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Despite all the advantages that cell-cultured influenza vaccines have over egg-based influenza vaccines, the inferior productivity of cell-culture systems is a major drawback that must be addressed. BST-2 (tetherin) is a host restriction factor which inhibits budding-out of various enveloped viruses from infected host cells. We developed BST-2-deficient MDCK and Vero cell lines to increase influenza virus release in cell culture. BST-2 gene knock-out resulted in increased release of viral particles into the culture medium, by at least 2-fold and up to 50-fold compared to release from wild-type counterpart cells depending on cell line and virus type. The effect was not influenza virus/MDCK/Vero-specific, but was also present in a broad range of host cells and virus families; we observed similar results in murine, human, canine, and monkey cell lines with viruses including MHV-68 (Herpesviridae), influenza A virus (Orthomyxoviridae), porcine epidemic diarrhea virus (Coronaviridae), and vaccinia virus (Poxviridae). Our results suggest that the elimination of BST-2 expression in virus-producing cell lines can enhance the production of viral vaccines. Biotechnol. Bioeng.2017;114: 2289-2297. © 2017 Wiley Periodicals, Inc.

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An unconventional BST-2 function: Down-regulation of transient protein expression

Cited by 9 publications

References 40 publications

Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus

Proteomic analysis reveals down-regulation of surfactant protein B in murine type II pneumocytes infected with influenza A virus

The avian influenza virus PA segment mediates strain-specific antagonism of BST-2/tetherin

Enhanced production of enveloped viruses in BST‐2‐deficient cell lines

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