Apical Gene Transfer into Quiescent Human and Canine Polarized Intestinal Epithelial Cells by Lentivirus Vectors

Seppen, Jurgen; Barry, Simon C.; Klinkspoor, J. H.; Katen, Louis J.; Lee, S. P.; Garcia, J. Victor; Osborne, W.R.A.

doi:10.1128/jvi.74.16.7642-7645.2000

Cited by 37 publications

(28 citation statements)

References 16 publications

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“…Polarized entry can be mediated by several mechanisms, such as differential distribution of viral receptors on apical and basolateral surfaces, inaccessibility or inactivation of viral receptors, and postentry factors inhibiting viral replication. The literature on VSV entry is controversial, with an early report demonstrating basolateral infection of MDCK cells (20) and more recent reports of the virus infecting airway epithelial and Caco-2 cells via the apical surface (8,40). This variation may reflect differences in the origin of the airway cells, culture conditions, and/or degree of polarization.…”

Section: Vol 82 2008 Role Of Polarization In Hcv Entry 467mentioning

confidence: 99%

“…In contrast, depleting Huh-7.5 cells of calcium had no effect on HCVpp or HCVcc infectivity, consistent with our observation that these cells do not form TJ-dependent paracellular barriers. Many viruses exhibit polarized routes of entry into primary and transformed epithelial cells, including vaccinia virus (37), VSV (8,20,40), human cytomegalovirus (18), Crimean-Congo hemorrhagic fever virus (12), coxsackievirus B, and adenovirus (14,15). Polarized entry can be mediated by several mechanisms, such as differential distribution of viral receptors on apical and basolateral surfaces, inaccessibility or inactivation of viral receptors, and postentry factors inhibiting viral replication.…”

Section: Vol 82 2008 Role Of Polarization In Hcv Entry 467mentioning

confidence: 99%

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Effect of Cell Polarization on Hepatitis C Virus Entry

Mee

Grove

Harris

et al. 2008

J Virol

104

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The primary reservoir for hepatitis C virus (HCV) replication in vivo is believed to be hepatocytes within the liver. Three host cell molecules have been reported to be important entry factors for receptors for HCV: the tetraspanin CD81, scavenger receptor BI (SR-BI), and the tight-junction (TJ) protein claudin 1 (CLDN1). The recent discovery of a TJ protein as a critical coreceptor highlighted the importance of studying the effect(s) of TJ formation and cell polarization on HCV entry. The colorectal adenocarcinoma Caco-2 cell line forms polarized monolayers containing functional TJs and was found to express the CD81, SR-BI, and CLDN1 proteins. Viral receptor expression levels increased upon polarization, and CLDN1 relocalized from the apical pole of the lateral cell membrane to the lateral cell-cell junction and basolateral domains. In contrast, expression and localization of the TJ proteins ZO-1 and occludin 1 were unchanged upon polarization. HCV infected polarized and nonpolarized Caco-2 cells to comparable levels, and entry was neutralized by anti-E2 monoclonal antibodies, demonstrating glycoprotein-dependent entry. HCV pseudoparticle infection and recombinant HCV E1E2 glycoprotein interaction with polarized Caco-2 cells occurred predominantly at the apical surface. Disruption of TJs significantly increased HCV entry. These data support a model where TJs provide a physical barrier for viral access to receptors expressed on lateral and basolateral cellular domains.Hepatitis C virus (HCV) is an enveloped positive-stranded RNA virus and the sole member of the Hepacivirus genus, within the family Flaviviridae. Worldwide, approximately 170 million individuals are infected with HCV and a significant fraction of these people are at risk of developing serious progressive liver disease. The principal reservoir for viral replication is believed to be hepatocytes within the liver. The recent development of the retrovirus pseudoparticle system (HCVpp) (5, 25) and the ability of the JFH-1 strain of HCV to release infectious particles in cell culture (HCVcc) (30,45,51) have allowed studies on the mechanism of HCV entry and replication.Viruses initiate infection by attaching to molecules or receptors on the cell surface. Expression and localization of these receptors are often important determinants of a cell's susceptibility to infection and of virus tropism for particular tissues. The observation that HCVpp only infect human liver-derived cell lines in vitro suggests that liver-specific receptors contribute to defining the hepatotropism of HCV. Current evidence suggests that at least three host cell molecules are important for HCV entry in vitro, i.e., the tetraspanin CD81 (5, 25, 35), scavenger receptor class B member I (SR-BI) (5,23,26,39), and tight-junction (TJ) protein claudin 1 (CLDN1) (19). Recent data suggest that CLDN6 and CLDN9 can also function as coreceptors allowing HCV entry (33, 50). HCV glycoproteins (gps) have been reported to interact directly with CD81 and SR-BI (reviewed in reference 11). Mutagenesis...

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Section: Vol 82 2008 Role Of Polarization In Hcv Entry 467mentioning

confidence: 99%

Section: Vol 82 2008 Role Of Polarization In Hcv Entry 467mentioning

confidence: 99%

Effect of Cell Polarization on Hepatitis C Virus Entry

Mee

Grove

Harris

et al. 2008

J Virol

104

View full text Add to dashboard Cite

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“…Transduction of the intestinal tract via liposomal [6], retroviral [7], lentiviral [8], herpes simplex viral [9] and adenoviral [10,11] vector systems has been previously demonstrated. Limited success has been achieved with these modalities either due to short duration of transgene expression or adverse host immune responses [12].…”

Section: Introductionmentioning

confidence: 99%

Gene Delivery to Intestinal Epithelial Cells In vitro and In vivo with Recombinant Adeno-Associated Virus Types 1, 2 and 5

et al. 2007

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Intestinal disorders such as inflammatory bowel disease (IBD) result in chronic illness requiring lifelong therapy. Our aim was to evaluate the efficacy of recombinant adeno-associated virus (AAV) vector-mediated gene delivery to intestinal epithelial cells in vitro and in vivo. Human colon epithelial cell lines and colon biopsies were transduced using AAV pseudotypes 2/1, 2/2, and 2/5 encoding green fluorescence protein (GFP). Mice were administered the same vectors through oral, enema, intraperitoneal (IP) injection and superior mesenteric artery (SMA) injection routes. Tropism and efficiency were determined by microscopy, flow cytometry, immunohistochemistry and PCR. Caco2 cells were more permissive to AAV transduction. Human colon epithelial cells in organ culture were more effectively transduced by AAV2/2. SMA injection provided the most effective means of vector gene transfer to small intestine and colonic epithelial cells in vivo. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript applicable for the investigation of IBD pathogenesis and novel therapeutic options, but also revealed the need for further studies to identify more efficient pseudotypes.

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“…Lentivirus was generated by cotransfection of 293T cells and titrated as described. 28 Transduction of CD34 ϩ CD38 Ϫ fetal liver cells with HIV-GFP was performed using fibronectin as described above for LZRS-IRES-GFP, except that the CD34 ϩ CD38 Ϫ cells were precultured overnight in the absence of cytokines.…”

Section: Retrovirus-and Lentivirus-mediated Gene Transfermentioning

confidence: 99%

Intrathymic and extrathymic development of human plasmacytoid dendritic cell precursors in vivo

Weijer

Uíttenbogaart

Voordouw

et al. 2002

Blood

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The development of plasmacytoid dendritic cells (pDC2) from human CD34 ؉ stem cells in vivo was studied in RAG-2 ؊/؊ interleukin (IL)-2R␥ ؊/؊ mice that lack functional T and B cells and natural killer cells. CD34 ؉ cells isolated from fetal liver or thymus were labeled with 5-and 6-carboxyfluorescein diacetate succinimidyl ester (CFSE) and were injected into a human thymus grafted subcutaneously in the RAG-2 ؊/؊ IL-2R␥ ؊/؊ mice. One to 4 weeks later the CFSE label was found not only in T cells but also in CD123 ؉/high CD4 ؉ CD45RA ؉ pDC2, indicating that the CD34 ؉ cells can develop into pDC2 within a thymus. In addition to pDC2, CFSElabeled dendritic cells with a mature phenotype, determined by the cell surface markers CD11c, CD83, and CD80, were found in the injected human thymus graft. pDC2 was not found in the periphery of mice carrying a human thymic graft, indicating that the intrathymic pDC2 failed to emigrate from the thymus. We also demonstrate that pDC2 can develop outside the thymus because relatively high percentages of pDC2 were found in the periphery after the intravenous injection of CD34 ؉ CD38 ؊ fetal liver cells in RAG-2 ؊/؊ IL-2R␥ ؊/؊ mice without a human thymus graft. These data indicate that the thymus and the peripheral pDC2 develop independently of each other. (Blood. 2002;99: 2752-2759

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Apical Gene Transfer into Quiescent Human and Canine Polarized Intestinal Epithelial Cells by Lentivirus Vectors

Cited by 37 publications

References 16 publications

Effect of Cell Polarization on Hepatitis C Virus Entry

Effect of Cell Polarization on Hepatitis C Virus Entry

Gene Delivery to Intestinal Epithelial Cells In vitro and In vivo with Recombinant Adeno-Associated Virus Types 1, 2 and 5

Intrathymic and extrathymic development of human plasmacytoid dendritic cell precursors in vivo

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