Elsevier

Virology

Volume 141, Issue 1, February 1985, Pages 119-129
Virology

Different murine cell lines manifest unique patterns of interference to superinfection by murine leukemia viruses

https://doi.org/10.1016/0042-6822(85)90188-6Get rights and content

Abstract

Interference to superinfection by murine leukemia viruses (MuLV) was analyzed in cells chronically infected with other MuLVs. A new sensitive focal immunofiuorescence assay employing monoclonal antibodies was used to detect foci of virus infection in live cell monolayers. Monoclonal antibodies were chosen which reacted with the challenge virus but not with the interfering virus. The results obtained confirmed some of the findings of previous workers using Moloney sarcoma virus pseudotypes as challenge viruses on mouse and nonmouse cells. In addition, SC-1 mouse cells nonproductively infected with defective spleen focus-forming virus were found to be resistant to superinfection by recombinant dual-tropic viruses. Furthermore, results indicated that interference patterns between some pairs of viruses differed in different cell types. Thus, xenotropic MuLV blocked superinfection by recombinant dual-tropic viruses in SC-1 feral mouse cells, but not in two lines of NZB mouse cells. Also, in a Mus dunii tail fibroblast cell line some unique patterns of interference were observed. One ecotropic MuLV blocked infection by two xenotropic viruses and three recombinant dual-tropic viruses. Two other ecotropic viruses blocked infection by only one of the two xenotropic viruses tested. These two ecotropic viruses also differed from each other in their ability to block the three recombinant viruses. In addition, two strains of amphotropic MuLV also differed in their interference capacity. As expected, strain 1504A did not block any viruses tested, whereas strain 4070A surprisingly blocked one xenotropic and one ecotropic MuLV. The lack of homogeneity in interference patterns seen in the Mus dunii cells suggested either that a large number of heterogeneous virus receptors were present on this cell line or that interference in these cells might operate through a mechanism other than blocking of virus receptors by the envelope protein of the interfering virus.

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