136 research outputs found
Establishment of the antiviral state in alpha, beta interferon-resistant Friend cells treated with gamma interferon: induction of 67K protein kinase activity in absence of detectable 2-5A synthetase
Treatment with murine gamma-interferon (IFN) preparations of variant sublines of Friend leukemia cells resistant to the alpha, beta IFN-induced antiviral state (Affabris, E., Jemma, C., and Rossi, G.B. (1982) Virology 120, 441-452; Affabris, E., Romeo, G., Belardelli, F., Jemma, C., Mechti, N., Gresser, I., and Rossi, G. B. (1983) Virology 125, 508-512) results in the establishment of a bona fide antiviral state. In fact, gamma IFN preparations are able to induce a dose-dependent reduction of endogenous virus release and of vesicular stomatitis or encephalomyocarditis viruses yields (up to 1.5 log). Under these experimental conditions, no inducible 2-5A synthetase activity is detectable in cell extracts. The 67-kDa protein kinase, uninducible by treatment with alpha, beta IFN (up to 13,000 units/ml), is instead induced upon treatment with gamma IFN at a similar rate of activity as in wild-type Friend leukemia cells, both when assayed in solution and after immobilization on poly(rI) X poly(rC)-agarose
Interferons-alpha,beta and gamma-resistant Friend cell variants exhibiting receptor sites for Interferons but no induction of 2-5A synthetase and 67K protein kinase
A number of Friend leukemia cell variants with a interferon-gamma (IFN-gamma)-resistant phenotype have been isolated. They appear resistant to the antiproliferative action of IFN-gamma and to the induction of the antiviral state assessed by Friend leukemia virus release and vesicular stomatitis virus yield. Selection was performed via a prolonged exposure to increasing amounts of highly purified recombinant IFN-gamma of wild-type Friend cells or of variant clones thereof already resistant to IFN-alpha/beta (Affabris et al., 1982, Virology 120, 441-452). Only the clones derived from IFN-alpha/beta-resistant variants showed a phenotype fully resistant to IFN-gamma treatment while keeping their previously acquired resistance to IFN-alpha/beta. These cells are not deficient in high-affinity receptors for IFN-gamma so that their resistant phenotype appears to be mediated by events distal to binding of IFN-gamma to its receptors. Furthermore, analysis of IFN-induced dsRNA-dependent 2-5A synthetase and 67K protein kinase enzymatic activities, biochemical markers for cellular responses to IFN, showed that both these activities were not induced in IFN-alpha/beta and IFN-gamma-resistant clones when treated with either type of IFN. Accordingly, no increased expression of 2-5A synthetase mRNA(s) could be detected by probing poly(A)+-enriched RNA from cells exposed to IFN-alpha/beta or IFN-gamma treatment with murine or human specific cDNAs. On the other hand, no major changes in restriction patterns of 2-5A synthetase gene(s) were observed in these variant cells by restriction endonuclease digestion and Southern blotting. In addition, analysis of 2-5A synthetase mRNA induction, performed on wild-type cells, showed that the kinetic of induction due to IFN-gamma treatment is slower than that obtained with IFN-alpha/beta
Introduction to the special issue: extracellular vesicles and biological signal delivery in the inflammatory microenvironment
2',5'-oligoadenylate synthetase-uninducible alpha, beta interferon-resistant Friend cells develop an antiviral state when permeabilized with lysolecithin and treated with 2',5'- oligoadenylate oligomers
Variant sublines of Friend erythroleukemia cells (FLC) that do not respond to alpha/beta-interferon (IFN-alpha/beta) by developing an antiviral state but respond partially to IFN-gamma with an induced antiviral state, lack the ability to induce the 2',5'-oligoadenylate (2-5A) synthetase pathway. Exposure of wild-type and variant cells to exogenous 2-5A oligomers made permeable with lysolecithin resulted in 50-70% inhibition of protein synthesis. Further, the replication of vesicular stomatitis virus in IFN-resistant 2-5A synthetase-deficient FLC exposed to 2-5A trimer was inhibited to the same extent as in wild-type cells. Last, a significant cleavage of ribosomal RNA was observed in samples of total RNAs extracted from variant and wild-type permeabilized FLC, but only if they were exposed to 2-5A. These data are compatible with the conclusion that (i) the activation of the 2-5A-dependent endoribonuclease is not impaired in the variant cells, and (ii) the uninducibility of 2-5A synthetase can be bypassed by exogenously introducing its products, which leads to the establishment of a bona fide antiviral state
Nef, the shuttling molecular adaptor of HIV, influences the cytokine network
Several viruses manipulate host innate immune responses to avoid immune recognition and improve viral replication and spreading. The viral protein Nef of Human Immunodeficiency Virus is mainly involved in this "hijacking" activity and is a well established virulence factor. In the last few years there have been remarkable advances in outlining a defined framework of its functions. In particular Nef appears to be a shuttling molecular adaptor able to exert its effects both on infected and non infected bystander cell. In addition it is emerging fact that it has an important impact on the chemo-cytokine network. Nef protein represents an interesting new target to develop therapeutic drugs for treatment of seropositive patients. In this review we have tried to provide a unifying view of the multiple functions of this viral protein on the basis of recently available experimental data
Friend virus-induced erythroleukemia: a model system to study erythroid differentiation and leukemia development
Since 1957, studies of Friend erythroleukemia have contributed greatly to research focused on erythroid differentiation, oncogenic retroviruses, and leukemia development. Infection with the Friend virus complex interferes with both proliferation and differentiation of the erythroid compartment. In reviewing this system, recent results concerning (1) sensitivity to erythropoietin and activation of the erythropoietin receptor during Friend-virus induced tumorigenicity, (2)oncogene and tumor suppressor genes expression, and (3) modulation of expression of transferring receptor and ferritin during the course of Friend erythroleukemia cells differentiation have been analysed. These results have furthered our understanding of both erythroleukemia development as well as the control mechanism(s)of cell growth and erythroid differentiation
Subcellular distribution of 2' 5' oligoadenylate synthetase in differentiating Friend leukemia cells.
Interactions of interferon with in vitro model systems involved in hematopoietic cell differentiation.
- …
