Dual susceptibility of a 3T3 mouse cell line to infection by N‐ and B‐tropic murine leukemia virus: Apparent lack of expression of the FV‐1 gene

Gisselbrecht, S; Bassin, Robert H.; Gerwin, Brenda I.; Rein, Alan

doi:10.1002/ijc.2910140113

Cited by 55 publications

(28 citation statements)

References 30 publications

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“…LLC-MK2 cells may have lost expression of the restriction factor. A precedent exists for cell lines from restricting mice lacking restriction in SC1 cells and 3T3FL cells (23,24). Further analysis of factor expression will require isolation of the gene or genes responsible.…”

Section: Discussionmentioning

confidence: 99%

Restriction of lentivirus in monkeys

Besnier

Takeuchi

Towers

2002

Proc. Natl. Acad. Sci. U.S.A.

264

274

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Retroviruses are able to cross species barriers and have done so many times throughout evolution. Perhaps as a consequence, dominant mechanisms have arisen to block infection by murine retroviruses in mice (restriction factor Fv1) and humans (restriction factor Ref1), as well as in other mammals. Here we describe a block to HIV and simian immunodeficiency virus in monkeys. Like previously described restrictions the block is saturable and gives rise to multiple-hit infection kinetics. Furthermore, like restriction of murine leukemia virus in humans, the block is before reverse transcription. Intriguingly, African green monkey cells are able to block both HIV and simian immunodeficiency virus, and each virus is able to saturate and abrogate the restriction of the other, suggesting that a common factor is responsible.

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Section: Discussionmentioning

confidence: 99%

Restriction of lentivirus in monkeys

Besnier

Takeuchi

Towers

2002

Proc. Natl. Acad. Sci. U.S.A.

264

274

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“…Laboratory-adapted MLV strains, such as Moloney MLV, proliferate equally well in Fv1 n or Fv1 b cells, exhibiting N/B-tropism. Cells carrying a nonrestrictive allele, referred to as Fv1 0 , allow infection by both N-and B-tropic MLV (24,27,43,44). Fv1 exerts its antiretroviral effect at a postentry step, after reverse transcription and prior to integration (37,76).…”

mentioning

confidence: 99%

“…Mouse cells express the factor Fv1 (47,56,58), which is present in several allelic forms that specifically restrict infection by certain strains of MLV (48) (24,27,43,44). Fv1 exerts its antiretroviral effect at a postentry step, after reverse transcription and prior to integration (37,76).…”

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confidence: 99%

Murine T Cells Potently Restrict Human Immunodeficiency Virus Infection

Baumann

Unutmaz

Miller

et al. 2004

J Virol

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Development of a mouse model for human immunodeficiency virus type 1 (HIV-1) infection has advanced through the progressive identification of host cell factors required for HIV-1 replication. Murine cells lack HIV-1 receptor molecules, do not support efficient viral gene expression, and lack factors necessary for the assembly and release of virions. Many of these blocks have been described using mouse fibroblast cell lines. Here we identify a postentry block to HIV-1 infection in mouse T-cell lines that has not been detected in mouse fibroblasts. While murine fibroblastic lines are comparable to human T-cell lines in permissivity to HIV-1 transduction, infection of murine T cells is 100-fold less efficient. Virus entry occurs efficiently in murine T cells. However, reduced efficiency of the completion of reverse transcription and nuclear transfer of the viral preintegration complex are observed. Although this block has similarities to the restriction of murine retroviruses by Fv1, there is no correlation of HIV-1 susceptibility with cellular Fv1 genotypes. In addition, the block to HIV-1 infection in murine T-cell lines cannot be saturated by a high virus dose. Further studies of this newly identified block may lend insight into the early events of retroviral replication and reveal new targets for antiretroviral interventions.Murine cells are refractory to human immunodeficiency virus type 1 (HIV-1) replication at multiple stages of the viral life cycle. While this has allowed a finer inspection of the role of various host factors in HIV-1 replication, it has been an impediment to the development of a genetically modified mouse permissive to HIV-1 infection. A number of host factors have been identified that are indispensable for replication of HIV-1. Necessary factors absent in murine T cells include the human forms of the HIV-1 receptor and coreceptor molecules, CD4 and CCR5, whose murine orthologs do not support HIV-1 entry (10). In contrast, the murine form of CXCR4 can be utilized as a coreceptor by HIV-1 (7, 69). Postentry, human cyclin T1 is necessary for efficient Tat-mediated transactivation of the HIV-1 long terminal repeat (LTR) (22). Additional blocks in later steps of the HIV-1 life cycle in murine cells include excessive splicing of HIV-1 genomic RNA (49) and defects in Rev function (72). Aberrant splicing of HIV-1 mRNA appears to be partially corrected by the human splice inhibitor p32 (80). HIV-1 particle assembly is also impaired in murine cells (6,53). This restriction can be overcome by fusion of murine cells with human cells, suggesting that murine cells lack a factor (or factors) necessary for HIV-1 Gag assembly and release (52). Substitution of the HIV-1 matrix (MA) region with that of murine leukemia virus (MLV) also circumvents this block, supporting the notion that species-specific cofactors are critical for virion assembly and release (13,63).Not only do mouse cells lack some of the factors necessary for HIV-1 replication, they also express factors that actively interfere with retrovira...

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“…The neutralizing activity of anti-gp70 serum was checked against Gross MuLV produced by D55-Gross cells, a clone of D55-3T3-F1 chronically infected with Gross virus (Gisselbrecht et al, 1974). Tissue culture supernatant fluid (1 ml) was incubated at 37 °C, for 2 h, with various amounts of serum.…”

Section: Short Communicationmentioning

confidence: 99%

“…Singlecell suspensions were prepared from the liver of individual embryos or from pooled spleens of embryos of the same litter, and virus production was studied using two methods. The cells were plated onto mouse NB-type indicator cells (3T3 F1 clone 5D) (Gisselbrecht et aL, 1974) and the number of virus-producing cells was determined using the infectious centre assay developed by Melief et al (1975). In a parallel assay, granulocyte-macrophage progenitor ceils (or colonyforming cells: GM-CFC) were stimulated to differentiate in vitro by plating the cells in semisolid medium containing horse serum and granulocyte-macrophage colony-stimulating factor (GM-CSF) from mouse lung-conditioned medium (Sheridan & Metcalf, 1973).…”

mentioning

confidence: 99%