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Evidence against expression of an endogenous murine leukemia virus causing cellular resistance to lysis by activated

L R Gooding1, J R Taylor, S M Laster

  • 1Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322.

Insights

Murine leukemia virus (MuLV) expression in transformed cells does not solely cause resistance to macrophage lysis. Further research is needed to determine if MuLV is necessary for this resistance.

Area of Science:

  • Immunology
  • Virology
  • Cell Biology

Background:

  • Previous studies linked macrophage resistance in murine fibroblast cell lines to gp70 expression of endogenous ecotropic murine leukemia virus (MuLV).
  • The role of MuLV expression in conferring resistance to macrophage-mediated cytolysis was not fully understood.

Purpose of the Study:

  • To directly investigate a causative relationship between MuLV expression and resistance to macrophage lysis.
  • To determine if MuLV expression is sufficient to induce a macrophage-resistant phenotype in transformed cells.

Main Methods:

  • Northern blot analysis to detect retroviral RNA in macrophage-resistant cells.
  • Monoclonal antibody (mAb) analysis to identify the host-range class of MuLV gp70.
  • Isolation and characterization of ecotropic MuLV from resistant cells.
  • Infection of macrophage-sensitive cell lines with isolated MuLV and subsequent testing for sensitivity to macrophage cytolysis.

Main Results:

  • Macrophage-resistant cells contained full-length retroviral RNA and expressed non-recombinant ecotropic gp70.
  • Infection of macrophage-sensitive cell lines with ecotropic MuLV did not confer resistance to macrophage lysis.
  • MuLV-infected cells maintained high levels of cell surface gp70 and released infectious MuLV but remained sensitive to lysis.

Conclusions:

  • Expression of murine leukemia virus (MuLV) alone is not sufficient to induce resistance to macrophage-mediated cytolysis in transformed murine fibroblast cell lines.
  • While MuLV expression may be necessary for the development of macrophage resistance, it does not appear to be the sole causative factor.

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