Effect of the Fv‐1 gene on leukemia virus in mouse cell heterokaryons

Tennant, Raymond W.; Myer, F. E.; McGrath, Lorraine

doi:10.1002/ijc.2910140410

Cited by 22 publications

(17 citation statements)

References 35 publications

(15 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similarly, Fv1 (Friend virus susceptibility factor 1) restricts retroviral infection at a postbinding stage prior to integration and formation of proviral structures (25). Fv1-mediated restriction is dominant in hybrid cells formed between cells infected with the appropriate virus but lacking this restrictive factor and Fv1-expressing cells (28). In contrast, hybrid cells formed between cells expressing factors that restrict viral entry and cells lacking these factors restore virus entry.…”

Section: Discussionmentioning

confidence: 99%

Primate Gammaretroviruses Require an Ancillary Factor Not Required for Murine Gammaretroviruses To Infect BHK Cells

Eiden

2011

J Virol

View full text Add to dashboard Cite

BHK cells remain resistant to xenotropic murine retrovirus-related virus (XMRV) or gibbon ape leukemia virus (GALV) infection, even when their respective receptors, Xpr1 or PiT1, are expressed. We set out to determine the stage at which viral infection is blocked and whether this block is mediated by a dominantnegative factor or the absence of a requisite ancillary factor. BHK cells bind neither XMRV nor GALV envelope proteins. BHK cells expressing the appropriate receptors bind XMRV or GALV envelope proteins. BHK cells can be infected by NZB-XMV(New Zealand Black mouse xenotropic murine virus)-enveloped vectors, expressing an envelope derived from a xenotropic retrovirus that, like XMRV, employs Xpr1 as a receptor, and also by vectors bearing the envelope of 10A1 murine leukemia virus (MLV), a murine retrovirus that can use PiT1 as a receptor. The retroviral vectors used in these analyses differ solely in their viral envelope proteins, suggesting that the block to XMRV and GALV infection is mediated at the level of envelope-receptor interactions. N-linked glycosylation of the receptors was not found to mediate resistance of receptor-expressing BHK cells to GALV or XMRV, as shown by tunicamycin treatment and mutation of the specific glycosylation site of the PiT1 receptor. Hybrid cells produced by fusing BHKXpr1 or BHKPiT1 to XMRV-or GALV-resistant cells, respectively, can mediate efficient XMRV or GALV infection. These findings indicate that BHK cells lack a factor that is required for infection by primate xenotropic viruses. This factor is not required for viruses that use the same receptors but were directly isolated from mice.

show abstract

Section: Discussionmentioning

confidence: 99%

Primate Gammaretroviruses Require an Ancillary Factor Not Required for Murine Gammaretroviruses To Infect BHK Cells

Eiden

2011

J Virol

View full text Add to dashboard Cite

show abstract

“…Genetic analysis has revealed that the Fv-1 gene is located on chromosome 4 of the mouse (4). The Fv-1 gene restriction of MuLV can also be demonstrated in mouse cell cultures in vitro (5,6) and, by a somatic cell fusion technique, was shown to be dominantly expressed in the heterokaryons (7). The precise mechanism of action of Fv-1 gene on MuLV is still unknown.…”

mentioning

confidence: 99%

Transfection of Fv-1 permissive and restrictive mouse cells with integrated DNA of murine leukemia viruses.

Hsu¹,

Yang²,

Tennant³

et al. 1978

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

View full text Add to dashboard Cite

Whole-cell DNA preparations isolated from SC-1 cells chronically infected with N-or B-tropic murine leukemia viruses (MuLV) were tested for infectious activity in an Fv-1n (NIH-3T3) and two Fv-1 b (C57BL/6 and SV-A31) cell cultures. Efficiency of transfection for all DNAs was better in the NIH-3T3 cells than in C57BL/6 or SV-A31 cells; and an [N-tropic MuLVJSC- (Clinton, TN), respectively. All cells used were within 10 passages of the original sources and were grown in Eagle's minimal essential medium containing 10% heat inactivated fetal calf serum, streptomycin (100;g/ml), and penicillin (100 units per ml).DNA Preparations. SC-1 cells were inoculated with N-or B-tropic MuLV at a multiplicity of infection of 1. Forty-eight hours later they showed more than 90% infection by immunofluorescence measurement. After five serial passages in dishes, the chronically infected SC-1 cells were grown to confluency in medium containing hydrocortisone (1 ,uM) and insulin (0.1 international unit/ml) in 6 X 75 cm roller bottles. The cells were harvested by scraping, washed, and used for DNA isolation according to a modification of Marmur's method (12), which includes Pronase digestion, ribonuclease digestion, and extractions with chloroform/isoamyl alcohol, 25:1 (vol/vol), as described (13,11). The final DNA products were dissolved in 15 mM NaCI/1.5 mM Na citrate, pH 7.0, and stored in aliquots at -70°. DNA concentration was measured spectrophotometrically at 260 nm by assuming that 20 A20 units equal 1 mg of DNA. All DNA preparations showed A 2m/A28o ratios of 1.9-2.0.Infectious DNA Assay. The detailed procedure for DNA transfection in mouse cell cultures has been described (11). In this study, all cultures were plated at 2 X 105 cells per 35-mm dish 20 hr prior to DNA inoculation. The cells, with medium removed, were exposed to 0.3 ml of the freshly prepared calcium DNA suspension (14) which contained various doses of sample DNA and also an appropriate amount of calf thymus DNA to maintain a constant DNA concentration of 40 Ag/ml. After 15 min, 3 ml of medium was added and the dishes were placed in a 370 CO2 incubator for an additional 15 hr before DNA was removed by a change to fresh medium. Two to 3 days after DNA inoculation, when the cultures became confluent, the cells were trypsinized and used 1:5 for subculture. Serial Abbreviations: MuLV, murine leukemia virus; PFU, plaque-forming units.

show abstract

“…Studies on the mechanism of the Fv-i restriction have shown that the inhibition is intracellular (8)(9)(10)(11). Analysis of the fate of virus in heterokaryons of permissive and nonpermissive cells indicated that the restriction functions at some early postpenetration step in infection (I1).…”

mentioning

confidence: 99%

“…The host-range specificity of the virus stocks was (letermine(l by titration on N-and B3-type cells (11 18 hr, the cells were treated with DEAE-D for 1 hr, washed, and the respective cell extract added for 2 hr.…”

mentioning

confidence: 99%

Reciprocal Inhibition of Mouse Leukemia Virus Infection by Fv-1 Allele Cell Extracts

Tennant

Schluter

Yang

et al. 1974

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

Self Cite

View full text Add to dashboard Cite

show abstract

Effect of the Fv‐1 gene on leukemia virus in mouse cell heterokaryons

Cited by 22 publications

References 35 publications

Primate Gammaretroviruses Require an Ancillary Factor Not Required for Murine Gammaretroviruses To Infect BHK Cells

Primate Gammaretroviruses Require an Ancillary Factor Not Required for Murine Gammaretroviruses To Infect BHK Cells

Transfection of Fv-1 permissive and restrictive mouse cells with integrated DNA of murine leukemia viruses.

Reciprocal Inhibition of Mouse Leukemia Virus Infection by Fv-1 Allele Cell Extracts

Contact Info

Product

Resources

About