Besmer, Peter and Baltimore, David (1977) Mechanism of restriction of ecotropic and xenotropic murine leukemia viruses and formation of pseudotypes between the two viruses. Journal of Virology, 21 (3). pp. 965-973. ISSN 0022-538X http://resolver.caltech.edu/CaltechAUTHORS:BESjvir77
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Ecotropic and xenotropic murine leukemia viruses (MuLV's) constitute separate interference groups; within each group there is cross-interference, but between the groups there is no detectable interference. Interference is manifest against pseudotypes in which the vesicular stomatitis virus genome is contained within the coat of one of the murine leukemia viruses. The pseudotypes display the cell specificity of the leukemia viruses: pseudotypes with an ecotropic MuLV coat infect mouse cells but not rabbit or mink cells; pseudotypes with a xenotropic MuLV coat infect rabbit or mink cells well but mouse cells very poorly. Efficient pseudotype formation also occurs between the two MuLV classes, and both the interference patterns and the cell specificity of these pseudotypes are entirely determined by their envelope. Using these pseudotypes, ecotropic MuLV infection could be established in xenogeneic cells, and the resulting progeny could be scored by using a conventional XC cell assay. Also, xenotropic MuLV infection could be established in a mouse cell, showing that no absolute intracellular barrier against xenotropic virus growth exists in murine cells. The major barriers against both xenotropic and ecotropic MuLV therefore are cell surface barriers. Xenogeneic cells probably lack receptors for ecotropic MuLV, but murine cells may either lack receptors for xenotropic MuLV or have receptors that are blocked by endogenous expression of the glycoprotein of endogenous xenotropic MuLV.
|Additional Information:||Copyright © 1977 by the American Society for Microbiology. Received for publication 1 September 1976 We thank Anne Cotellessa for excellent technical assistance. We are grateful to Jay Levy both for sharing with us his early observations on xenotropic murine leukemia virus, which led to the work presented here, and for providing cell lines and antisera. We are also grateful to Alice Huang for supplying viruses and antisera and for discussion. This work was supported by grant VC-4G from the American Cancer Society and Public Health Service grant CA-14051 from the National Cancer Institute. P.B. was supported by a fellowship from the Schweizerischer Nationalfonds 831.266.74 and by National Research Service Award CA05083 from the National Cancer Institute. D.B. is a Research Professor of the American Cancer Society.|
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|Deposited On:||06 Apr 2006|
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