In vitro replication and cytopathogenicity of the feline immunodeficiency virus for feline t4 thymic lymphoma 3201 cells

Tochikura, Tatsurokuro; Hayes, Kathleen; Cheney, Carolyn; Tanabe-Tochikura, Akiko; Rojko, Jennifer L.; Mathes, Lawrence E.; Olsen, Richard G.

doi:10.1016/0042-6822(90)90323-j

Cited by 24 publications

(17 citation statements)

References 16 publications

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“…FIV can infect multiple human cell lines resulting in proviral integration [152] [60,105,223] and at least two different strains of FIV (Petaluma and V1-CSF) can productively infect primary human PBMC and macrophages in vitro [115]. While the percentage of cells expressing FIV genes is significantly lower in human PBMC than in feline PBMC (12% versus > 90%) indicating a restriction in the type of cells infected and/or reduced replication efficiency, in vitro infection results in the production of infectious supernatant, increased reverse transcriptase activity, and detection of FIV genomic material for at least 21 days [115].…”

Section: Host Rangementioning

confidence: 99%

Transmission and Immunopathogenesis of FIV in Cats as a Model for HIV

Burkhard

Dean²

2003

CHR

119

139

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The feline immunodeficiency virus (FIV) model provides a system to study lentivirus transmission, virus kinetics, pathogenesis, host responses, and immune dysfunction in a natural, out-bred host, under controlled conditions with specific-pathogen-free animals. The diversity of primary FIV strains can be exploited to mirror the range of disease manifestations associated with HIV infection. FIV is infectious via intravenous, intraperitoneal, intradermal, or subcutaneous injection as well as by atraumatic instillation onto the oral, vaginal, or rectal mucosa. Together, these features allow investigators to model specific aspects of HIV infection in a highly relevant and relatively inexpensive animal model. Well-developed areas of the FIV model include: (1) transmission of cell-associated as well as cell-free virus; (2) mucosal infectivity and immunopathogenesis; (3) vertical transmission; (4) acquired immunodeficiency including defects of the innate immune system; (5) thymic dysfunction; (6) neurotropism and neuropathogenesis; (7) host-virus interactions and the role of specific gene products; (8) efficacy of antiviral therapy; and (9) efficacy and immune correlates of experimental vaccines. This review will encompass areas specific to transmission and immunopathogenesis.

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Section: Host Rangementioning

confidence: 99%

Transmission and Immunopathogenesis of FIV in Cats as a Model for HIV

Burkhard

Dean²

2003

CHR

119

139

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“…This result shows that each HCV in serum samples has a different ability for viral propagation in IMY-N9 cells. Then, we attempted to estimate viral activity using TCID 50 in IMY-N9, as has been shown for other viruses 32,33 and "TCI 50 HCV RNA", which we used as a marker for how many copies of HCV RNA are required for 50% tissue culture infection. First, we compared the TCID 50 and TCI 50 HCV RNA values of 2 HCVs, which released into the media of primary hepatocyte culture derived from an HCV-infected patient 18 and stayed in liver tissue homogenates derived from the same patient.…”

Section: Establishment Of Hybrid Cell Lines Between Human Hepatocytesmentioning

confidence: 99%

Acquisition of susceptibility to hepatitis C virus replication in HepG2 cells by fusion with primary human hepatocytes: Establishment of a quantitative assay for hepatitis C virus infectivity in a cell culture system

et al. 2001

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Hepatitis C virus (HCV) replicates in human and chimpanzee hepatocytes. To characterize the nature of HCV and evaluate antiviral agents, the development of an HCV replication system in a cell culture is essential. We developed a cell line derived from human hepatocytes by fusing them with a hepatoblastoma cell line, HepG2, and obtained several clones. When we tested the clones for their ability to support HCV replication by nested RT-PCR, we found 1 clone (IMY-N9) that was more susceptible to HCV replication than HepG2. The negative-strand HCV RNA was detected in IMY-N9 by strand-specific RT-PCR, and viral RNA was identified in culture supernatant during the culture. Hepatitis C virus (HCV) is now recognized as the principal agent in parentally transmitted non-A, non-B hepatitis. HCV is a single-stranded positive-sense RNA virus of about 9,500 nucleotides (nt) that encodes a large polyprotein, 1,2 which is processed into viral structural and nonstructural proteins. Recently, full-length HCV RNA transcripts from HCV cDNAs were shown to be infectious in chimpanzees. 3,4,5 Although our understanding of the molecular biology of HCV has progressed rapidly, little is known about its biological characteristics, because in vivo studies have been limited to the studies performed using chimpanzees that have been infected or transfected with HCV. The development of efficient animal cell culture systems for HCV or readily available animal models are priorities for the study of HCV. HCV replication has been described based on studies of liver tissue and peripheral blood mononuclear cells (PBMC) from infected patients. 6,7 Animal cell culture systems for HCV replication have been developed from human T and B cell lines, 8,9,10 human fetal liver cells, 11,12 and chimpanzee primary hepatocytes. 13 Efficient long-term viral replication, however, has not been reported in any system. HCV replication may be stringently restricted to differentiated hepatocytes, which may have receptors for HCV on their cell surface and specific factors to support viral growth. Recently, a host cellular factor, polypyrimidine-tract-binding protein (PTB), was reported to bind the HCV 3Ј-end, and was thought to be a cis-acting element for HCV replication. 14,15 PTB is also related to the mechanism of HCV translational regulation, 16,17 indicating that several cellular factors may be involved in the mechanism of HCV propagation. We previously reported that HCV replicated efficiently in primary cultured human hepatocytes, 18 and another group also confirmed our findings. 19 However, we still need to develop a more convenient cell-culture system because it is difficult to obtain a constant source of human hepatocytes. In this study, we fused human hepatocytes with a hepatoblastoma cell line, HepG2, and obtained hybrid cell lines. We then tested the ability of the hybrids to support HCV replication by monitoring HCV RNA titers in cultured cells using a real-time detection PCR (RTD-PCR). 20 The results showed that several hybrid cell lines were more suscept...

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“…4(A)). This phenomenon has also been observed when FIV-Petaluma was passaged through 3201 cells (Tochikura et al, 1990), though expanded host-cell range was not described.…”

Section: Phenotypic Changes Associated With Il-2 Independencementioning

confidence: 74%

“…The T-cell lines 104-C1 and 104-C7 were isolated from an FIV negative cat. The lymphoma cell line, 3201, (Tochikura et al, 1990) was obtained from Dr. William Hardy. The two continuous IL-2-independent cell lines, MCH5-4DL and 104-C1DL were isolated from their parental lines, MCH5-4 and 104-C1, respectively, after undergoing crisis in the absence of interleukin-2 and Con-A.…”

Section: Cell Lines and Viruses And Propagation Methodsmentioning

confidence: 99%

FIV infection of IL-2-dependent and -independent feline lymphocyte lines: Host cells range distinctions and specific cytokine upregulation

Lerner¹,

Grant²,

Parseval³

et al. 1998

Veterinary Immunology and Immunopathology

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We have analyzed the ability of three molecular clones of feline immunodeficiency virus (FIV) and an ex vivo variant to infect nine distinct specific-pathogen-free feline cell lines in tissue culture. The purpose of these studies was to elucidate mechanisms by which host cells regulate the level of virus infection and expression and to assess host cell cytokine responses to virus infection. Cells used for the analyzes included four IL-2-dependent continuous T-cell lines (104-C1, 104-C7, MCH5-4 and DB FeTs) which arose from long-term passage, followed by limiting dilution cloning of peripheral blood mononuclear cells (PBMCs); two IL-2-independent T-cell lines (104-C1DL and MCH5-4DL) which originated from two of the IL-2-dependent lines, 104-C1 and MCH5-4; respectively; Crandell feline kidney cells (CrFK); G355-5 brain-derived glial cells; and the T-cell lymphoma line, 3201. Cells were infected with FIV-PPR, FIV-34TF10, FIV 34TF10orf2rep, and a variant arising from FIV-PPR during ex vivo passage on 104-C1DL cells, termed FIV-PPRglial. Infection of the IL-2-dependent T-cell line, 104-C1, by FIV-PPR resulted in the specific and distinct upregulation of cytokine expression. In particular, these cells doubled their expression of the pleiotropic cytokines, interleukin-4 and interleukin-12 after FIV infection. Interferon-gamma production also increased after infection with FIV whereas, TNFalpha expression remained constant. Also, a marked upregulation of MHC class II expression was noted post infection of MCH5-4 and 104-C1 cells with FIV-PPR. Similar results were obtained after infection with FIV-34TF10orf2rep, indicating that the upregulation of cytokine expression is not an isolate-specific phenomenon. Changes in cytokine and class II expression are similar to various reports for the in vivo cytokine alterations in FIV, SIV and HIV infections. The ex vivo infection of these cell lines offers amanipulable system to examine the mechanism(s) by which lentiviruses alter cytokine expression.

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In vitro replication and cytopathogenicity of the feline immunodeficiency virus for feline t4 thymic lymphoma 3201 cells

Cited by 24 publications

References 16 publications

Transmission and Immunopathogenesis of FIV in Cats as a Model for HIV

Transmission and Immunopathogenesis of FIV in Cats as a Model for HIV

Acquisition of susceptibility to hepatitis C virus replication in HepG2 cells by fusion with primary human hepatocytes: Establishment of a quantitative assay for hepatitis C virus infectivity in a cell culture system

FIV infection of IL-2-dependent and -independent feline lymphocyte lines: Host cells range distinctions and specific cytokine upregulation

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