Characteristics of murine C‐type viruses. I. Independent assortment of infectivity in one <i>in vivo</i> and four <i>in vitro</i> assays

Fenyõ, Éva Mária; Grundner, Gertrud

doi:10.1002/ijc.2910120216

Cited by 16 publications

(7 citation statements)

References 18 publications

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“…There was no correlation between the malignant behavior of the cell lines and production of focusforming virus. The virus produced by the highly malignant A9HT, unlike the parental A9, has previously been shown to be unable to induce focus formation (17). A9HT and A9G-TG100 A12 did produce infectious L virus.…”

Section: Resultsmentioning

confidence: 92%

In vitro derived mouse A9 cell clones differing in malignancy: analysis by somatic cell hybridization with YACIR lymphoma cell clones.

Clements¹,

Fenyõ²,

Klein³

1976

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

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A culture of mouse A9 cells yielded clones of both high and low malignancy. Confirmation of the differences in malignancy of the clones was obtained after their hybridization with subclones of YACIR, a lymphoma induced by Moloney leukemia virus. Low malignant A9 clones suppressed the malignancy of the YACIR partner in the hybrids. Hybrids between a highly malignant A9 clone and two different clones of YACIR "complemented" to yield hybrids of reduced malignancy.No correlation was found between the malignancy of a particular A9 clone and its ability to produce a focus-forming mouse C-type virus.A9, a variant of mouse L cells deficient in hypoxanthine/guanine phosphoribosyltransferase (HGPRT) (1), has been used extensively as a parental cell in the analysis of malignancy by somatic cell hybridization (2, 3). The standard A9 subline used is of low malignancy and has been fused with a variety of highly malignant murine tumors. Such hybrids are of low malignancy when inoculated into x-irradiated syngeneic newborn mice so long as the hybrid retains all or nearly all the chromosomes of both parental cells. These data are consistent with the presence in the low malignant cells of genetic information whose expression is incompatible with tumor formation. If such information is lost, or its expression is blocked, a highly malignant subline can develop.Fluctuation in the take incidence of L cells passaged in culture over many years has been reported (4), but conclusive evidence for the simultaneous presence of cells of both high and low malignancy within a single cultured cell line has not previously been documented. Highly malignant variants of L cells (4) and of A9 (A9HT) (5) (7,8).Somatic Cell Hybridization. Beta propiolactone-inactivated Sendai virus was used to fuse the cells essentially as described (9). The hybrid cells originated as single colonies, one colony only being taken from a particular bottle.Cell Cloning. A9 cells were cloned either by suspension in 0.3% agarose-containing medium at a density of 10 cells per ml (10) or in liquid culture in petri dishes with an initial inoculum of five cells per 60 mm petri dish. One clone only was subsequently picked from each dish.Chromosome Preparation. Metaphase spreads were prepared essentially as described (11) and stained with Giemsa.Test for Malignancy. Viable cells (1 X 105) were inoculated to x-irradiated (4 J/kg) syngeneic newborn mice. Mice were scored for tumor formation (a "take") during the 3 subsequent months, after which the experiment was terminated. Animals not developing tumors by this time were scored as negative. with phosphate-buffered saline and infected with 0.5 ml volumes of virus dilutions. The virus source was cell culture supernatant that had been passed through a Millipore filter of 0.45 ,m pore size. The virus was allowed to adsorb to the cells for 60 min at 370 and then the cultures were rinsed with medium. The medium was changed every third day. The cultures were observed at days 7, 10, and 17 for morphologically altered foci accordi...

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Section: Resultsmentioning

confidence: 92%

In vitro derived mouse A9 cell clones differing in malignancy: analysis by somatic cell hybridization with YACIR lymphoma cell clones.

Clements¹,

Fenyõ²,

Klein³

1976

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

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“…The YAC and YA7C lymphomas were induced by inoculating Moloney leukemia virus (MLV) to newborn A and (A × C57BI)FI mice, respectively (9). The characteristics of YAC cellsurface antigens and virus production have been described in a series of publications (6,10,11). Both tumors were maintained in the ascites form in syngeneic mice.…”

Section: Methodsmentioning

confidence: 99%

“…Like other L-cell sublines, A9HT produces a C-type virus that shows a certain resemblance to endogenous mouse viruses. It is N-tropic (10,11,13) and lacks leukemogenic activity (14,15). In the XC test, it induces distinct syncytia rather than plaques (16).…”

Section: Methodsmentioning

confidence: 99%

Immunization of mice with syngeneic Moloney lymphoma cells induces separate antibodies against virion envelope glycoprotein and virus-induced cell surface antigens.

Fenyõ¹,

Yefenof²,

Klein³

et al. 1977

The Journal of Experimental Medicine

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Immunization of mice with heavily irradiated syngeneic Moloney lymphoma cells evokes antibodies against the major viral envelope antigen, gp71, and the Moloney virus-induced cell surface antigen (MCSA). A9HT cells, an L-cell subline, react with the antibodies against the viral envelope antigen only; this reaction can be completely inhibited by virus or purified gp71. Reactivity to Moloney lymphoma cells (YAC) was only partially inhibited (maximum 30%) or not at all. This can be attributed to the reaction of the YAC cells with antibodies directed against MCSA, a nonvirion cell surface component according to both biological and biochemical evidence. Antibody-induced capping of gp71 or p15(E) did not change the membrane distribution of MCSA or H-2, indicating that these antigens represent distinct entities on the cell surface. MCSA showed only minimal capping and thereby differed in behavior from both H-2 and virion antigens. gp71 could be capped by the mouse antiserum as revealed by subsequent staining with monospecific anti-gp71 antiserum. Under ordinary test conditions this reactivity is overshadowed by the reaction against MCSA. The lack of MCSA capping reflects a difference in anchorage of this antigen.

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“…The L virus differs from MLV with regard to leukemogenesis, plaque-formation (it is negative for both) and host cell tropism, being N-tropic in contrast to MLV which is NB-tropic. Furthermore, the L virus, like MLV, infects JLS-V9 cells and induces foci on BALB/3T3 cells (Fenyo and Grundner, 1973).…”

Section: The A9 Cellmentioning

confidence: 99%

“…Preparation of the test samples. The test samples were prepared in the same way as described previously (Fenyo and Grundner, 1973).…”

Section: Assavs For Virus Infectivitymentioning

confidence: 99%

Characteristics of murine C‐type viruses. IV. The virus produced by ehrlich tumor cells and its hybrids with mouse L cells

Grundner¹,

Fenyõ²,

Klein³

1974

Intl Journal of Cancer

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The iiijertious properties of viruses produced by Ehrlich tumor cells ( E ) , the A9 ,srth/irie of' mouse L cc#s ( L ) , their hj-brids ( E L , arid E L ) und high-maligtiarit suhlincs yf' the low-maligtiant hybrid line (EL,,, i W P r C investigated. The infectivity a.s.say.s wen' utitigetr induction ow JLS-V9 cells, antigenic cotiversion und focus iriductioii otr S I L wlls ( D.56 .subhe) unc/.focus .formatioti oti BAL Bl3 T3 cells. The E and L viruses, pro-rlrrrc~d by the pavetitul cells, were detected irr the JLS-V9 test but were distitiguished in S 1 L ~~~ urid BALBI3T3 cells. The L virus wus ,focus-positive, the E virus .focustiegutive ( B A L B/3T3). For utitiAwiic cotiversion, the L virus was negutive and the E virus positive ( D S 6 ) . The hybrid cell line, tested 011 sevi~rctl occasions after the hydridizatioti evetit, produced viruses with characteristics similur to both E arid L viruses, riyurcllc'ss of the complete or rerlucd chromosome numbers. The muligriunt sublines selected from the hybrid showed pryferetrtial loss of' the A9 puretit-derived biarmed chromosomes. Otie of thi.se lities produced virus (EL,,,) with infective properties similur to those of' the E virus. This suggests thut the virus produced by u particular cell line is determitred by the cell getlome. Another maligtiutit subline was .fourid to hi, ncycrtive .for productiotr of ii1fi.ctiou.s virus in all three indicator systems.The infectious properties of viruses produced in hybrid cells, resulting from the fusion of Moloney lymphomas and L cells (A9 subline) were reported previously (Fenyo et ul., 1971(Fenyo et ul., , 1973. The viruses produced by the parental ( Y .Yr and L) and hybrid cells (YL and YrL) were characterized by a panel on infectivity assays. These assays did not give concordant results when different viruses were used, allowing the infec-

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Characteristics of murine C‐type viruses. I. Independent assortment of infectivity in one in vivo and four in vitro assays

Abstract: The infective properties of mouse C-type viruses produced by two Moloney lymphoma lines, mouse L cells ( A 9 and A9HTsublines)

Cited by 16 publications

References 18 publications

In vitro derived mouse A9 cell clones differing in malignancy: analysis by somatic cell hybridization with YACIR lymphoma cell clones.

In vitro derived mouse A9 cell clones differing in malignancy: analysis by somatic cell hybridization with YACIR lymphoma cell clones.

Immunization of mice with syngeneic Moloney lymphoma cells induces separate antibodies against virion envelope glycoprotein and virus-induced cell surface antigens.

Characteristics of murine C‐type viruses. IV. The virus produced by ehrlich tumor cells and its hybrids with mouse L cells

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