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Analysis of interactions of DNA polymerase beta and reverse transcriptases of human immunodeficiency and mouse leukemia viruses with dNTP analogs containing a modified sugar residue.

https://arctichealth.org/en/permalink/ahliterature7171
Source
Biochemistry (Mosc). 2005 Jan;70(1):1-7
Publication Type
Article
Date
Jan-2005
Author
N A Lebedeva
T A Seredina
V N Silnikov
T V Abramova
A S Levina
S N Khodyreva
N I Rechkunova
O I Lavrik
Author Affiliation
Institute of Chemical Biology and Fundamental Medicine, Siberian Division of the Russian Academy of Sciences, Novosibirsk 630090, Russia.
Source
Biochemistry (Mosc). 2005 Jan;70(1):1-7
Date
Jan-2005
Language
English
Publication Type
Article
Keywords
Catalysis
DNA Polymerase beta - antagonists & inhibitors - metabolism
DNA Repair - drug effects
DNA, Viral - biosynthesis
Deoxyribonucleotides - metabolism - pharmacology
HIV-1 - enzymology
HIV-1 Reverse Transcriptase - antagonists & inhibitors - metabolism
Kinetics
Moloney murine leukemia virus - enzymology
Morpholines - metabolism - pharmacology
RNA-Directed DNA Polymerase - metabolism
Recombinant Proteins
Research Support, Non-U.S. Gov't
Reverse Transcriptase Inhibitors - metabolism - pharmacology
Structure-Activity Relationship
Abstract
Substrate properties of various morpholinonucleoside triphosphates in the reaction of DNA elongation catalyzed by DNA polymerase beta, reverse transcriptase of human immunodeficiency virus (HIV-1 RT), and reverse transcriptase of Moloney murine leukemia virus (M-MuLV RT) were compared. Morpholinonucleoside triphosphates were utilized by DNA polymerase beta and HIV-1 reverse transcriptase as substrates, which terminated further synthesis of DNA, but were virtually not utilized by M-MuLV reverse transcriptase. The kinetic parameters of morpholinoderivatives of cytosine (MorC) and uridine (MorU) were determined in the reaction of primer elongation catalyzed by DNA polymerase beta and HIV-1 reverse transcriptase. MorC was a more effective substrate of HIV-1 reverse transcriptase and significantly less effective substrate of DNA polymerase beta than MorU. The possible use of morpholinonucleoside triphosphates as selective inhibitors of HIV-1 reverse transcriptase is discussed.
PubMed ID
15701045 View in PubMed
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Differential increase in topoisomerase II in simian virus 40-infected cells.

https://arctichealth.org/en/permalink/ahliterature4154
Source
J Virol. 1990 Feb;64(2):918-21
Publication Type
Article
Date
Feb-1990
Author
R. Rainwater
K. Mann
Author Affiliation
Biology Department, University of Alaska, Anchorage 99508.
Source
J Virol. 1990 Feb;64(2):918-21
Date
Feb-1990
Language
English
Publication Type
Article
Keywords
Animals
Antigens, Polyomavirus Transforming - genetics
Cell Line
Cell Transformation, Viral
DNA Replication
DNA Topoisomerases, Type I - biosynthesis
DNA Topoisomerases, Type II - biosynthesis
DNA, Viral - biosynthesis
Kinetics
Research Support, U.S. Gov't, P.H.S.
Simian virus 40 - enzymology - genetics - immunology
Abstract
The time course of expression of topoisomerase I, topoisomerase II, and simian virus 40 (SV40) large tumor (T) antigen was determined in whole-cell extracts of uninfected versus SV40-infected TC7 cells. After a minor increase, the level of topoisomerase I remained fairly constant throughout the time course in both uninfected and SV40-infected cells. In contrast, the level of topoisomerase II increased markedly in SV40-infected cells but not in uninfected cells following the appearance of SV40 T antigen.
PubMed ID
2153253 View in PubMed
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Passive transfer of antiviral antibodies restricts replication of Aleutian mink disease parvovirus in vivo.

https://arctichealth.org/en/permalink/ahliterature5874
Source
J Virol. 1989 Jan;63(1):9-17
Publication Type
Article
Date
Jan-1989
Author
S. Alexandersen
S. Larsen
A. Cohn
A. Uttenthal
R E Race
B. Aasted
M. Hansen
M E Bloom
Author Affiliation
Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840.
Source
J Virol. 1989 Jan;63(1):9-17
Date
Jan-1989
Language
English
Publication Type
Article
Keywords
Acute Disease
Aleutian Mink Disease - prevention & control
Aleutian Mink Disease Virus - genetics - immunology - physiology
Animals
Antibodies, Viral - analysis
Chronic Disease
DNA, Viral - biosynthesis
Immunization, Passive - veterinary
Mink
Nucleic Acid Hybridization
Parvoviridae - immunology
Pulmonary Fibrosis - pathology - prevention & control - veterinary
Research Support, Non-U.S. Gov't
Viremia - veterinary
Virus Replication
Abstract
When mink kits were infected neonatally with a highly virulent strain of Aleutian disease virus (ADV), 100% of both Aleutian and non-Aleutian genotype mink died of interstitial pneumonia characterized by permissive ADV infection of alveolar type II cells. Treatment of infected kits with either mink anti-ADV gamma globulin or mouse monoclonal antibodies against ADV structural proteins reduced mortality by 50 to 75% and drastically reduced the severity of clinical signs. Interestingly, mink kits that survived the acute pulmonary disease all developed the chronic form of immune complex-mediated Aleutian disease. Thus, the antibodies directed against ADV structural proteins were capable of modulating the in vivo pathogenicity from an acute fulminant disease to a chronic immune complex-mediated disorder. The mechanism of this modulation was examined by strand-specific in situ hybridization. We found that the number of ADV-infected type II cells was the same in both untreated and antibody-treated kits. However, in the treated kits, viral replication and transcription were restricted at the cellular level. These data suggested that antibodies prevented acute viral pneumonia by restricting the intracellular level of viral replication and that the relevant antigenic determinants were contained within the viral structural proteins. The restricted levels of viral replication and transcription seen in antibody-treated mink kits resembled the levels observed in infected adult mink and suggested a role of antiviral antibodies in development of persistent infection and chronic immune complex disease.
PubMed ID
2535756 View in PubMed
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