Effects of Organic Solvents on the Reverse Transcription Reaction Catalyzed by Reverse Transcriptases from Avian Myeloblastosis Virus and Moloney Murine Leukemia Virus

2010 ◽  
Vol 74 (9) ◽  
pp. 1925-1930 ◽  
Author(s):  
Kiyoshi YASUKAWA ◽  
Atsushi KONISHI ◽  
Kuniyo INOUYE
Keyword(s):  
Organic Solvents ◽  
Reverse Transcription ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Moloney Murine Leukemia Virus ◽  
Avian Myeloblastosis Virus ◽  
Reverse Transcriptases ◽  
Reverse Transcription Reaction ◽  
Murine Leukemia

Kuehneromycins A and B, Two New Biological Active Compounds from a Tasmanian Kuehneromyces sp. (Strophariaceae, Basidiomycetes)

1995 ◽  
Vol 50 (1-2) ◽  
pp. 1-10 ◽  
Author(s):  
Gerhard Erkel ◽  
Kirsten Lorenzen ◽  
Timm Anke ◽  
Robert Velten ◽  
Alberto Gimenez ◽  
...  
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Dna Polymerases ◽  
Competitive Inhibitor ◽  
Antimicrobial Activities ◽  
Moloney Murine Leukemia Virus ◽  
Strong Inhibitor ◽  
Avian Myeloblastosis Virus ◽  
Reverse Transcriptases ◽  
Murine Leukemia

Abstract In a search for new inhibitors of RNA-directed DNA-polymerases kuehneromycin A (1) was isolated from fermentations of a Tasmanian Kuehneromyces species. Its structure was elucidated by spectroscopic methods. Kuehneromycin A (1) is a non-competitive inhibitor of avian myeloblastosis virus (Ki 200 μᴍ) and moloney murine leukemia virus (Ki 40 μᴍ) reverse transcriptases. The second compound, kuehneromycin B (2) is a strong inhibitor of platelet aggregation stimulated with different inducers. In addition, both compounds exhibit cytotoxic and antimicrobial activities.

Hyphodontal, a New Antifungal Inhibitor of Reverse Transcriptases from Hyphodontia sp. (Corticiaceae, Basidiomycetes)

1994 ◽  
Vol 49 (9-10) ◽  
pp. 561-570 ◽  
Author(s):  
Robert Velten ◽  
Alberto Gimenez ◽  
Wolfgang Steglich
Keyword(s):  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Dna Polymerases ◽  
Competitive Inhibitor ◽  
Moloney Murine Leukemia Virus ◽  
Spectroscopic Methods ◽  
Avian Myeloblastosis Virus ◽  
Antifungal Activities ◽  
Reverse Transcriptases ◽  
Murine Leukemia

Abstract In a search for inhibitors of RNA-directed DNA polymerases a new isolactarane sesquiterpenoid, hyphodontal (1), was isolated from fermentations of a Canadian Hyphodontia species. Its structure was elucidated by spectroscopic methods. Hyphodontal strongly inhibits the growth of several yeasts and is a non-competitive inhibitor of avian myeloblastosis virus (Ki 346 μᴍ) and Moloney murine leukemia virus (Ki 112 μᴍ) reverse transcriptases. In addition, cytotoxic and antifungal activities were observed.

scholarly journals Inhibition of murine leukemia virus with poly-2'-O-(2,4-dinitrophenyl)poly[A].

1996 ◽  
Vol 40 (10) ◽  
pp. 2311-2317 ◽  
Author(s):  
M A Ashun ◽  
Y Hu ◽  
I Kang ◽  
C C Li ◽  
J H Wang
Keyword(s):  
Body Weight ◽  
Murine Leukemia Virus ◽  
Animal Studies ◽  
Leukemia Virus ◽  
Human Lymphocytes ◽  
Antiviral Drug ◽  
Inhibitory Effect ◽  
Moloney Murine Leukemia Virus ◽  
Reverse Transcriptases ◽  
Murine Leukemia

Poly-2'-O-(2,4-dinitrophenyl)poly[A] (DNP-poly[A] is a potent inhibitor of reverse transcriptases from a variety of sources (I. Kang and J. H. Wang, J. Biol. Chem. 269:12024-12031, 1994). In the present study, its inhibitory effect on the reverse transcriptase (RT) from Moloney murine leukemia virus (MuLV) was investigated. DNP-poly[A] was found to enter the virus spontaneously and to completely inhibit the RT within 30 min at 0 degree C. The inhibitor was also spontaneously transported into isolated human lymphocytes and leukocytes at 37 degrees C. Animal studies have demonstrated the effectiveness of DNP-poly[A] as an antiviral drug when administered intraperitoneally at various doses from 1 to 100 mg/kg of body weight. MuLV-infected mice show the presence of RT in their blood as well as increased numbers of leukocytes. After the administration of DNP-poly[A] at a dosage of 100 mg/kg of body weight three times a week over a 3-week period, RT could no longer be detected by an ultrasensitive RT-PCR assay. Autopsy showed that the spleens of infected but untreated mice were enlarged 2- to 10-fold, with fused nodules and the proliferation of large abnormal lymphocytes, whereas the spleens of infected but treated mice resembled the normal spleens of uninfected control mice. These observations indicate that further study of DNP-poly[A] as a general antiretroviral agent is desirable.

scholarly journals Specific Cleavages by RNase H Facilitate Initiation of Plus-Strand RNA Synthesis by Moloney Murine Leukemia Virus

2003 ◽  
Vol 77 (9) ◽  
pp. 5275-5285 ◽  
Author(s):  
Sharon J. Schultz ◽  
Miaohua Zhang ◽  
James J. Champoux
Keyword(s):  
Dna Synthesis ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Rnase H ◽  
Primer Extension ◽  
Moloney Murine Leukemia Virus ◽  
Cleavage Sites ◽  
Reverse Transcriptases ◽  
Hybrid Substrates ◽  
Murine Leukemia

ABSTRACT Successful generation, extension, and removal of the plus-strand primer is integral to reverse transcription. For Moloney murine leukemia virus, primer removal at the RNA/DNA junction leaves the 3′ terminus of the plus-strand primer abutting the downstream plus-strand DNA, but this 3′ terminus is not efficiently reutilized for another round of extension. The RNase H cleavage to create the plus-strand primer might similarly result in the 3′ terminus of this primer abutting downstream RNA, yet efficient initiation must occur to synthesize the plus-strand DNA. We hypothesized that displacement synthesis, RNase H activity, or both must participate to initiate plus-strand DNA synthesis. Using model hybrid substrates and RNase H-deficient reverse transcriptases, we found that displacement synthesis alone did not efficiently extend the plus-strand primer at a nick with downstream RNA. However, specific cleavage sites for RNase H were identified in the sequence immediately following the 3′ end of the plus-strand primer. During generation of the plus-strand primer, cleavage at these sites generated a gap. When representative gaps separated the 3′ terminus of the plus-strand primer from downstream RNA, primer extension significantly improved. The contribution of RNase H to the initiation of plus-strand DNA synthesis was confirmed by comparing the effects of downstream RNA versus DNA on plus-strand primer extension by wild-type reverse transcriptase. These data suggest a model in which efficient initiation of plus-strand synthesis requires the generation of a gap immediately following the plus-strand primer 3′ terminus.

scholarly journals Interaction of Moloney Murine Leukemia Virus Capsid with Ubc9 and PIASy Mediates SUMO-1 Addition Required Early in Infection

2006 ◽  
Vol 80 (1) ◽  
pp. 342-352 ◽  
Author(s):  
Andrew Yueh ◽  
Juliana Leung ◽  
Subarna Bhattacharyya ◽  
Lucy A. Perrone ◽  
Kenia de los Santos ◽  
...  
Keyword(s):  
Binding Site ◽  
Reverse Transcription ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Moloney Murine Leukemia Virus ◽  
Viral Gene ◽  
Alanine Scanning Mutagenesis ◽  
Viral Dna ◽  
Murine Leukemia

ABSTRACT Yeast two-hybrid screens led to the identification of Ubc9 and PIASy, the E2 and E3 small ubiquitin-like modifier (SUMO)-conjugating enzymes, as proteins interacting with the capsid (CA) protein of the Moloney murine leukemia virus. The binding site in CA for Ubc9 was mapped by deletion and alanine-scanning mutagenesis to a consensus motif for SUMOylation at residues 202 to 220, and the binding site for PIASy was mapped to residues 114 to 176, directly centered on the major homology region. Expression of CA and a tagged SUMO-1 protein resulted in covalent transfer of SUMO-1 to CA in vivo. Mutations of lysine residues to arginines near the Ubc9 binding site and mutations at the PIASy binding site reduced or eliminated CA SUMOylation. Introduction of these mutations into the complete viral genome blocked virus replication. The mutants exhibited no defects in the late stages of viral gene expression or virion assembly. Upon infection, the mutant viruses were able to carry out reverse transcription to synthesize normal levels of linear viral DNA but were unable to produce the circular viral DNAs or integrated provirus normally found in the nucleus. The results suggest that the SUMOylation of CA mediated by an interaction with Ubc9 and PIASy is required for early events of infection, after reverse transcription and before nuclear entry and viral DNA integration.

scholarly journals Characterization of Intracellular Reverse Transcription Complexes of Moloney Murine Leukemia Virus

1999 ◽  
Vol 73 (11) ◽  
pp. 8919-8925 ◽  
Author(s):  
Ariberto Fassati ◽  
Stephen P. Goff
Keyword(s):  
Reverse Transcription ◽  
Murine Leukemia Virus ◽  
Leukemia Virus ◽  
Sedimentation Velocity ◽  
Micrococcal Nuclease ◽  
Moloney Murine Leukemia Virus ◽  
Velocity Sedimentation ◽  
Equilibrium Density ◽  
Transcription Complexes ◽  
Murine Leukemia

ABSTRACT To examine the early events in the life cycle of Moloney murine leukemia virus (MoMLV), we analyzed the intracellular complexes mediating reverse transcription. Partial purification of the reverse transcription complexes (RTCs) by equilibrium density fractionation and velocity sedimentation indicated that three distinct species of intracellular complexes are formed shortly after cell infection. Only one of these species is able to start and complete reverse transcription in the cell cytoplasm. This RTC is composed of at least the viral genome, capsid, integrase, and reverse transcriptase proteins. The RTC becomes permeable to micrococcal nuclease but not to antibodies. Shortly after initiation of reverse transcription, the viral strong stop DNA within the RTC is protected from nuclease digestion. The sedimentation velocity of the RTC decreases during reverse transcription. After entry into the nucleus, most capsid proteins are lost from the RTC and its sedimentation velocity decreases further.

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