Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

BL/VL3 radiation leukemia virus (RadLV) is a thymotropic, highly leukemogenic murine leukemia virus (MuLV) which is unable to replicate in vitro in mouse fibroblasts. We have previously reported that the U3 long terminal repeat region of its genome is responsible for this block (E. Rassart, Y. Paquette, and P. Jolicoeur, J. Virol. 62:3840-3848, 1988). By using hybrids of permissive and resistant cells infected with BL/VL3 RadLV or fibrotropic MuLV, we found that the resistant phenotype was dominant. Investigation to determine at which step of the virus cycle the block operates revealed that integration, transcription, and translation of the BL/VL3 viral genome occurred at normal levels in nonpermissive cells. The BL/VL3 RadLV Pr65gag proteins made in nonpermissive cells were also myristylated and located at the membrane, and the levels of their cleaved products were similar to those of fibrotropic MuLV. However, processing of BL/VL3 RadLV Pr85env was impaired in nonpermissive cells. Virions were not released into the culture medium of nonpermissive cells, as measured by reverse transcriptase activity and by content in p30 or gp70 protein and as documented by lower levels of budding particles seen by electron microscopy. These results indicate that BL/VL3 RadLV replication is blocked at a late stage of the virus cycle, i.e., at virion assembly. Interestingly, these BL/VL3 RadLV-infected nonpermissive fibroblasts were resistant to superinfection by fibrotropic Moloney MuLV, and this resistance also occurred at a late step of the Moloney virus cycle. Since this block is dominant, it appears that the U3 long terminal repeat region of the BL/VL3 viral genome has the ability to induce a cellular suppressor factor(s), thus bringing intracellular immunity against itself and against other ecotropic MuLVs.
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PMID:U3 long terminal repeat-mediated induction of intracellular immunity by a murine retrovirus: a novel model of latency for retroviruses. 143 13

We have analyzed the RNA genome of RadLV/VL3, a highly oncogenic murine leukemia virus. This virus is produced by a permanent cell line derived from a radiation leukemia virus-induced thymic lymphoma of C57BL/Ka mice. Two distinct RNA components were found in the virions: a 70S dimer containing two 8 kb RNA subunits and a 54S dimer containing two 5.6 kb RNAs. A nononcogenic retrovirus, BL/Ka(B), endogenous in the same strain of mice, contains only 8 kb viral RNA subunits. The linkages between both RadLV/VL3 dimers have identical thermal stabilities. Both dimers can serve as primer templates for reverse transcriptase and both produce very similar "strong-stop" cDNAs 147 +/- 1 bases long. Sequences at the 5' end of the 5.6 kb subunit contain the genes for the viral proteins p15 and p12, but the gene for p30 is either absent or partially deleted. In vitro translation of the 5.6 kb RNA yields a 100,000 molecular weight protein containing antigenic determinants which react with antibody to p15 but not with antibody to p30. In addition, cells producing RadLV/VL3 virus synthesize a novel of 1.6 kb poly(A)-containing cytoplasmic RNA which shows very little if any homology with BL/Ka(B) viral sequences.
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PMID:Radiation leukemia virus contains two distinct viral RNAs. 624 93