Isolation of a Sindbis virus variant by passage on mouse plasmacytoma cells

Abstract

A variant of Sindbis virus has been isolated by growing a stock of virus, previously passaged on chicken embryo cells, in mouse plasmacytoma (MOPC 31a) cells in suspension culture. An indirect immunofluorescence test and infective center assay showed that only a small fraction of cells could be infected by the stock wild-type virus, but that the population of virus accumulating after a few passages on the mouse cells had host-range properties distinct from the stock virus. The mouse-passaged virus retained its virulence for the original host and back-passaging of this virus on chicken cells did not change its newly acquired properties. Thus, this variant appears to be a genetically distinct form of Sindbis that adsorbs to and grows much better than the stock virus on several types of mouse cells including cultures of mouse macrophages.

Restricted replication of two alphaviruses in ricin-resistant mouse L cells with altered glycosyltransferase activities

“…Growth of viruses. Sindbis virus used in these experiments was a substrain selected for its ability to grow in the mouse plasmacytoma line MOPC 315 (28). It also exhibits enhanced infection of mouse L cells relative to the wild-type virus.…”

Defective mutant of Sindbis virus with a smaller-molecular-weight form of the E1 glycoprotein

“…A variant of the virus that grows better on mouse cells has been isolated simply by passaging stock virus in mouse plasmacytoma cells (24). These data suggest that stocks of virus comprise several genetically distinct forms that, although present in low concentrations, can be specifically selected for in the process of cloning or by passaging on different cells.…”

Domains of Virus Glycoproteins

“…Neutralizing antibodies are mainly directed against the E2 glycoprotein (Roehrig, 19861, but some monoclonal antibodies directed against epitopes on E l have neutralizing activity (Schmaljohn et al, 1983;Boere et al, 1984). A change in the ionic charge of the surface of Sindbis virus can have a profound effect on the host range of the virus (Symington and Schlesinger, 1975). The mutations that led to changes in the host range and surface charge of the variant were located in both E l and E2, but the precise place in the primary sequence was not determined (Symington and Schlesinger, 1978).…”