Use of VSV-G Pseudotyped Retroviral Vectors to Target Murine Osteoprogenitor Cells

Kalajzić, Ivo; Stover, Mary Louise; Liu, P.; Kalajzić, Žana; Rowe, David W.; Lichtler, Alexander C.

doi:10.1006/viro.2001.0903

Cited by 45 publications

(24 citation statements)

References 38 publications

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“…Disorders of these cells lead to bone diseases, such as osteopetrosis, osteosclerosis, and osteoporosis (15). Adenovirus and VSVG pseudotype retrovirus vectors can transduce foreign genes into some osteocytes in vitro and in vivo (2,14,21). The infectivities of VSVG-modified baculoviruses are also higher than those of the recombinant baculovirus possessing excess gp64 envelope protein.…”

Section: Discussionmentioning

confidence: 99%

In Vitro and In Vivo Gene Delivery by Recombinant Baculoviruses

Tani¹,

Lim²,

Yap

et al. 2003

J Virol

174

141

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Section: Discussionmentioning

confidence: 99%

In Vitro and In Vivo Gene Delivery by Recombinant Baculoviruses

Tani¹,

Lim²,

Yap

et al. 2003

J Virol

174

141

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“…The plasmids pCMV-⌬R8.74 (42), pcz-VSV-G (43), and derivatives of pWPI (carrying the genes of interest and in addition either the blasticidin S deaminase gene of Aspergillus terreus or a puromycin N-acetyltransferase gene) (44) or pLenti (encoding miR-122) (40) were transfected at a ratio of 3:1:3 into 293T cells. Lentiviral particles were harvested at 48 h posttransfection.…”

Section: Methodsmentioning

confidence: 99%

Apolipoprotein E Codetermines Tissue Tropism of Hepatitis C Virus and Is Crucial for Viral Cell-to-Cell Transmission by Contributing to a Postenvelopment Step of Assembly

Hueging

Doepke

Vièyres

et al. 2014

J Virol

100

114

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cHepatitis C virus (HCV) predominantly infects human hepatocytes, although extrahepatic virus reservoirs are being discussed. Infection of cells is initiated via cell-free and direct cell-to-cell transmission routes. Cell type-specific determinants of HCV entry and RNA replication have been reported. Moreover, several host factors required for synthesis and secretion of lipoproteins from liver cells, in part expressed in tissue-specific fashion, have been implicated in HCV assembly. However, the minimal cell type-specific requirements for HCV assembly have remained elusive. Here we report that production of HCV trans-complemented particles (HCV TCP ) from nonliver cells depends on ectopic expression of apolipoprotein E (ApoE). For efficient virus production by full-length HCV genomes, microRNA 122 (miR-122)-mediated enhancement of RNA replication is additionally required. Typical properties of cell culture-grown HCV (HCVcc) particles from ApoE-expressing nonliver cells are comparable to those of virions derived from human hepatoma cells, although specific infectivity of virions is modestly reduced. Thus, apolipoprotein B (ApoB), microsomal triglyceride transfer protein (MTTP), and apolipoprotein C1 (ApoC1), previously implicated in HCV assembly, are dispensable for production of infectious HCV. In the absence of ApoE, release of core protein from infected cells is reduced, and production of extracellular as well as intracellular infectivity is ablated. Since envelopment of capsids was not impaired, we conclude that ApoE acts after capsid envelopment but prior to secretion of infectious HCV. Remarkably, the lack of ApoE also abrogated direct HCV cell-to-cell transmission. These findings highlight ApoE as a host factor codetermining HCV tissue tropism due to its involvement in a late assembly step and viral cell-to-cell transmission. C urrently, around 160 million people are chronically infected with hepatitis C virus (HCV) worldwide (1). A prophylactic vaccine is not available, but direct-acting antivirals (DAA) have recently been approved for treatment (2). However, the novel triple therapy including pegylated alpha interferon (PEG-IFN-␣), ribavirin, and one of two available protease inhibitors is associated with side effects and is not licensed for all viral genotypes. A detailed understanding of the viral life cycle and the roles of specific viral and host factors may reveal novel targets for antiviral therapy and thus help to improve existing therapeutic options.Chronic HCV infection is a leading cause of liver disease, including hepatitis, liver cirrhosis, and hepatocellular carcinoma (3). It is also associated with numerous extrahepatic manifestations, such as cryoglobulenimia and neuronal disorders (reviewed in reference 4). While hepatocytes are thought to be the primary site of HCV replication, a number of studies have highlighted possible extrahepatic sites of replication, including peripheral blood mononuclear cells and cells of neuronal origin (reviewed in references 5 and 6). These observations sugge...

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“…The HuH6 cell lines were created by lentiviral gene transfer using the lentiviral self-inactivating vector pWPI-BSD (56) transducing individual CLDN1 genes and subsequent selection of transduced cells with DMEM complete supplemented with blasticidin (5 g/ml). Briefly, lentiviral particles were generated by cotransfection of the human immunodeficiency virus Gag-Pol expression construct pCMV-⌬R8.74 (19), the envelope protein expression construct pcz-VSV-G (27), and the respective lentiviral vector at a ratio of 3:1:3 into 293T cells (18) seeded 24 h prior to transfection at a density of 1.4 ϫ 10 6 /6-cm-diameter culture dish. Forty-eight hours later, the cell-free culture fluids were harvested and directly used to inoculate HuH6 cells.…”

Section: Methodsmentioning

confidence: 99%

Mouse-Specific Residues of Claudin-1 Limit Hepatitis C Virus Genotype 2a Infection in a Human Hepatocyte Cell Line

Haid

Windisch

Bartenschlager

et al. 2010

J Virol

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Recently, claudin-1 (CLDN1) was identified as a host protein essential for hepatitis C virus (HCV) infection.To evaluate CLDN1 function during virus entry, we searched for hepatocyte cell lines permissive for HCV RNA replication but with limiting endogenous CLDN1 expression, thus permitting receptor complementation assays. These criteria were met by the human hepatoblastoma cell line HuH6, which (i) displays low endogenous CLDN1 levels, (ii) efficiently replicates HCV RNA, and (iii) produces HCV particles with properties similar to those of particles generated in Huh-7.5 cells. Importantly, naïve cells are resistant to HCV genotype 2a infection unless CLDN1 is expressed. Interestingly, complementation of HCV entry by human, rat, or hamster CLDN1 was highly efficient, while mouse CLDN1 (mCLDN1) supported HCV genotype 2a infection with only moderate efficiency. These differences were observed irrespective of whether cells were infected with HCV pseudoparticles (HCVpp) or cell culture-derived HCV (HCVcc). Comparatively low entry function of mCLDN1 was observed in HuH6 but not 293T cells, suggesting that species-specific usage of CLDN1 is cell type dependent. Moreover, it was linked to three mouse-specific residues in the second extracellular loop (L152, I155) and the fourth transmembrane helix (V180) of the protein. These determinants could modulate the exposure or affinity of a putative viral binding site on CLDN1 or prevent optimal interaction of CLDN1 with other human cofactors, thus precluding highly efficient infection. HuH6 cells represent a valuable model for analysis of the complete HCV replication cycle in vitro and in particular for analysis of CLDN1 function in HCV cell entry.Hepatitis C virus (HCV) is a liver-tropic plus-strand RNA virus of the family Flaviviridae that has chronically infected about 130 million individuals worldwide. During long-term persistent virus replication, many patients develop significant liver disease which can lead to cirrhosis and hepatocellular carcinoma (54). Current treatment of chronic HCV infection consists of a combination of pegylated alpha interferon and ribavirin. However, this regimen is not curative for all treated patients and is associated with severe side effects (37). Therefore, an improved therapy is needed and numerous HCVspecific drugs targeting viral enzymes are currently being developed (47). These efforts have been slowed down by a lack of small-animal models permissive for HCV replication since HCV infects only humans and chimpanzees. Among small animals, only immunodeficient mice suffering from a transgene-induced disease of endogenous liver cells and repopulated with human primary hepatocytes are susceptible to HCV infection (39).The restricted tropism of HCV likely reflects very specific host factor requirements for entry, RNA replication, assembly, and release of virions. Although HCV RNA replication has been observed in nonhepatic human cells and even nonhuman cells, its efficiency is rather low (2,11,59,67). In addition, so far, efficient productio...

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Use of VSV-G Pseudotyped Retroviral Vectors to Target Murine Osteoprogenitor Cells

Cited by 45 publications

References 38 publications

In Vitro and In Vivo Gene Delivery by Recombinant Baculoviruses

In Vitro and In Vivo Gene Delivery by Recombinant Baculoviruses

Apolipoprotein E Codetermines Tissue Tropism of Hepatitis C Virus and Is Crucial for Viral Cell-to-Cell Transmission by Contributing to a Postenvelopment Step of Assembly

Mouse-Specific Residues of Claudin-1 Limit Hepatitis C Virus Genotype 2a Infection in a Human Hepatocyte Cell Line

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