Leukemia Rauscher virus

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. 

Schwendener RA, et al. New lipophilic acyl/alkyl dinucleoside phosphates as derivatives of 3 -azido-3 -deoxythymidine Inhibition of HIV-1 replication in vitro and antiviral activity against Rauscher leukemia virus infected mice with delayed treatment regimens. Antivir Res 1994 24 79. 

Pretazettine (395) has been the subject of numerous biological studies, and it has been shown to exhibit a number of interesting activities (96,97,101,178-187). For example, 395 was found to inhibit HeLa cell growth as well as protein synthesis in eukaryotic cells by interfering with the peptide bond formation step (97,101). Furthermore, pretazettine inhibited the purified RNA-dependent DNA polymerase (reverse transcriptase) from avian myeloblastosis virus, a typical C-type virus (178), in an unusual fashion since it physically combined with the polymerase enzyme itself rather than interacted with the nucleic acid template. Pretazettine also exhibited antiviral activity against the Rauscher leukemia virus in mouse embryo cell cultures by suppressing viral replication (179). 

Rauscher leukemia virus SOS induction = induction of an error-prone repair system TK = thymidine kinase... 

Narciclasine (22) halts protein synthesis by blockage of peptide-bond formation on the 60-S ribosomal subunit. The effect is specific for eucaryotic cells. Narciclasine inhibits Rauscher virus NIH/3T3 (Wink, 1993). Lycorine (8) blocks mitosis in the broad bean (Viciafaba). The mechanism appears to be related to inhibition of protein synthesis (Suffness and Cordell, 1985). Pretazettine (15) has been used in combination with DNA-binding and alkylating agents in the treatment of the Rauscher leukemia virus (Cordell, 1981 Martin, 1987). This alkaloid inhibits purified RNA-dependent DNA polymerase (reverse transcriptase) from avian myelo-... 

Polymers other than polynucleotides also have been found to induce interferon. Pyran-2-succinic anhydride, 4,5-dicar-boxy tetrahydro- 6-methyl- anhydride polymers in low daily doses protect mice infected with lethal doses of Friend or Rauscher leukemia virus. A correlation between degree of protection and interferon levels was noted. Vinyl sulfate polymers and divinyl ether-maleic acid copolymers induce interferon and protect mice against lethal virus infections. Both of these substances had activity that could not be accounted for by interferon alone. The dependency on molecular weight of polyacrylic acid polymers for interferon induction indicated a... 

Male CD-I mice Pb In drinking water, 0.004-0.1 M, starting 4 weeks of age Various viruses given l.p. 3-6 weeks after, including Rauscher leukemia virus and encephalomyocarditis virus Increased encephalomyocarditis virus mortality from Pb dosing up to 100% at 0.1 M Pb mouse interferon protective effect not reduced by Pb Gainer (1974)... 

Gainer, J.H., 1973. Activation of the Rauscher leukemia virus by metals. I. Natl. Cancer Inst. 51, 603-613. 

Fischer rat embryo Infected with Rauscher leukemia virus Focus on monolayer 40 45-49... 

With regard to the mechanism of its possible antiviral activity, we have observed an increase in interferon production by ascorbic acid following stimulation of mouse L cell cultures with poly (rI) poly (rC) (Siegel, 1975). We have also noted an enhancement of interferon production vivo following stimulation with Rauscher leukemia virus in BALB/c mice treated with 250 mg% L-ascorbic acid in the drinking water (Siegel, 1974). Thus, the antiviral activity of ascorbic acid may be due, in part, to enhanced interferon production however, the mechanism of this effect remains to be elucidated. 

Siegel, B. V, and Morton, J. I. (1970) Autoimmune disease in New Zealand Black mice infected with Rauscher leukemia virus. 

Although multi-acetylation reduced antibacterial activity, when streptovaricin C tri- and tetraacetates and streptovaricin G triacetate were tested against the reverse transcriptase of Rauscher leukemia virus (RLV), the acetylated compounds proved to be more active than the unacetylated or mono-acetylated streptovaricins. The atropisomers of the streptovaricin oligoacetates are also inactive as antibacterial agents or inhibitors of E. coli RNA polymerase but more active in inhibiting reverse transcriptase. The cyclic benzeneboronate and p-bromobenzeneboronate derivatives of streptovaricin C (11, 13, respectively) and atropisostrepto-varicin C (12, 1, respectively) triacetates, shown in Fig. 11, also inhibit reverse transcriptase but are inactive as antibacterial agents. 

Li, L. H., C. H. CowiE, L. G. Gray, D. M. Moran, T. D. Clark, and K. L. Rinehart, JR. Effects of Streptovaricins and Their Degradation Products on RNA-Directed DNA Polymerase of Rauscher Leukemia Virus. Submitted for publication. 

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