PubMed · 1438855
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A Iwamoto. 1992. [Host factors affecting retrovirus replication].. https://pubmed.ncbi.nlm.nih.gov/1438855/
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The Fv-1 murine gene controls predominantly the replication of leukemia viruses of murine cells. Forced passage by B-tropic Friend leukemia virus in the restrictive host cells (NIH, Fv-1n/n) results in viral progeny capable of replicating efficiently in murine cells of any Fv-1 type, which are denoted as NB-tropic virus. We have studied the RNase T1-resistant oligonucleotide pattern of a series of NB-tropic Friend virus isolates and have been able to show changes from the parental B-tropic virus which occur at the 5' end of the genome. Cloned NB-tropic virus falls into three classes, demonstrating either four, one, or no apparent changes in the genome. These results suggest the possibility that conversion to NB tropism occurs by a recombination mechanism but, since change to NB tropism can occur without any observable oligonucleotide alteration, they do not confirm that any single oligonucleotide is diagnostic of NB tropism.
Many different types of virus particles including avian retroviruses, Friend leukaemia virus and Sendai virus are able, when coincubated with human peripheral blood lymphocytes in the presence of mitogens or alloantigens, to inhibit the usual proliferative responses that normally ensue. These effects are independent of infection and can be obtained using u.v.-inactivated viruses as well as virus-lymphocyte combinations which are non-physiological in nature. Lymphocytes which are preincubated with viruses for as little as 5 min, and then washed free of unbound virus, are significantly impaired in terms of ability to react to mitogenic stimulus. These events may be mediated, in part at least, by the virus-induced elaboration by mononuclear cells of a factor with lymphocyte inhibitory potential.
Electron microscope and gel electrophoresis studies show that the high-molecular-weight (50 to 70S) RNA extract from Friend virus (FV) is a dimer with the same basic structure previously observed for the RNAs from RD-114 virus, baboon virus, and woolly monkey virus. This observation greatly strengthens the inference that the dimer structure is a general characteristic of the RNAs of all mammalian type C viruses. The FV dimer is slightly less stable than the RNA dimer of woolly monkey virus, which is, in turn, much less stable than those of RD-114 and baboon virus. There are three FV monomer components, small (S), medium (M), and large (L), with molecular lengths of 6.7 +/- 0.6, 7.7 +/- 0.6, and 9.5 +/- 0.6 kilobases, respectively. There are approximately equal amounts of the S and M components and much less of the L component. Most of the dimers are homodimers (SS, MM, and LL). The frequency of heterodimers (SM, SL, ML) is much less than expected for a random assortment model.