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Polycythaemia- and anaemia-inducing strains of spleen focus-forming virus differ in post-translational processing of envelope-related glycoproteins


A virus preparation was isolated by Friend which produced a rapid erythroblastosis in certain strains of mice1. Although the original virus preparation induced a slight anaemia in the terminal stages of the disease, other variants, derived from various in vivo and in vitro passages of the original virus, were associated with polycythaemia2,3, and the different viruses were accordingly classified as FVA (Friend virus anaemia-inducing) or FVP (Friend virus polycythaemia-inducing). Another important difference between the two strains is that whereas FVP induces in infected mice cells that are capable of forming colonies in vitro in the absence of erythropoietin4,5, colonies formed by cells derived from FVA-infected mice are erythropoietin dependent6–9. Differences were also noted in the amount of haemoglobin present in erythroid bursts produced after in vitro infection of haematopoietic cells with FVP or FVA22. Both FVA and FVP virus stocks have been shown to consist of at least two different viruses: the spleen focus-forming virus (SFFVP or SFFVA), a replication defective virus; and the Friend murine leukaemia virus (F-MuLV), a replication competent virus which acts as a helper virus for replication of the defective SFFV6,23. Here, in an attempt to correlate differences in the biological effects of the SFFVs derived from FVP and FVA stocks with biochemical properties of proteins encoded by them, we have compared the post-translational processing of the envelope glycoproteins encoded by these viruses, and have found both qualitative and quantitative differences in the processing of the envelope glycoproteins of the two virus stocks.

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