Friend murine leukemia virus

Fig. 11. Structures of oncoretrovirus receptor-binding domains. Left The receptorbinding domain of Friend murine leukemia virus (Fass et al, 1997). Right The homologous domain from subgroup B feline leukemia virus (Barnett et al, 2003). The positions of the variable subdomains and conserved /9-sandwich scaffold are indicated. The histidine residue critical for receptor binding-induced activation of membrane fusion by this virus group is indicated at the extreme amino terminus in the feline leukemia virus structure, but this residue was not seen in the electron density of the Friend receptor-binding domain.

Figure 1. Architecture of Friend murine leukemia virus. (A) Electron microscopic picture of F-MuLV particles (kindly donated by H. Frank, Max-Planck-lnstitute for Virus Research, Tubingen, Germany). (B) Schematic representation of the virion.

R. Geyer, J. Dabrowski, U. Dabrowski, D. Linder, M. Schluter, H.-H. Schott, S. Stirm, Oligosaccharides at individual glycosylation sites in glycoprotein 71 of Friend murine leukemia virus, Eur. J. Biochem., 1990, 187, 95-110. 

PMEA and its congeners are more effective in vivo than could be predicted from their in vitro potency. While less potent as an antiretrovirus agent than AZT in vitro, PMEA proved clearly superior to AZT when the two drugs were compared for their effectiveness in vivo, in mice infected with murine Moloney sarcoma virus [51,52]. PMEA was also shown to be effective against various other retrovirus infections, including Friend leukemia virus (FLV), Rauscher leukemia virus (RLV), and LP-BM5 (murine AIDS) virus infection in mice, feline leukemia virus (FeLV) or feline immunodeficiency virus (FIV) infection in cats, and SIV infection in macaque (rhesus) monkeys (for review, see Ref. 53). In the latter model [54], again PMEA proved far superior to AZT in suppressing several parameters of the disease. 

The antiretrovirus properties of NO were shown in mice infected with Friend leukemia virus, a murine retrovirus. NO produced by NO-generating compounds or activated macrophages inhibits viral replication in fibroblast cultures, and is involved in defens against this murine retrovirus in vivo [134]. It was also reported that NO donors can inhibit HIV-1 replication in human monocytes through induction ofiNOS [135],... 

The route of pyran administration is important, because intravenous pyran can stimulate Friend leukemia virus activity in contrast to intraperitoneal pyran, which is inhibitory (Schuller, Morahan, and Snodgrass, 1973). Paradoxically, certain murine sarcoma virus induced tumors are stimulated by pyran as well as other interferon inducers (Gazdar et al, 1972). This stimulation may be related to the ability of pyran to induce hepato-splenomegaly or splenomegaly in normal mice. 

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