Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.7 (DNA polymerase)
 17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although the origin of viruses has not yet been clarified, definite differences in evolutionary patterns have been found among RNA. Retro and DNA viruses. These differences are reflected in infectious diseases. RNA viruses, which have RNA in their genome, replicate many times over in cells within a short period of time, destroying the host cells and causing an acute infection. As the error frequency of RNA replicase enzymes is high, the rate of evolution of RNA viruses is very rapid. Retroviruses also contain RNA as their genome, but the genome RNA is reversely transcribed to the DNA in nuclei and then incorporated into the host chromosome to replicate. The error frequency of reverse transcriptase is also high, and therefore mutations easily occur as well. The transcribed DNA is integrated into host DNA in the nucleus, and it remains in the integrated state for human entire life time, causing chronic disease or developing malignant tumors. As DNA viruses except poxviruses replicate inside the cell nucleus and the error frequency of DNA polymerase is low, the speed of mutation and the degree of resulting diversity are lower than those in the case of the RNA virus. DNA viruses tend to stay inside the body for long periods of time and easily become latent. In this paper, I shall discuss 1) the nature of viruses, 2) the origin of viruses, 3) mutation and recombination, 4) diversity of RNA viruses, 5) quickly changing viral diseases, 6) eradicated viral diseases, 7) chronic and malignant diseases, and 8) control of viral diseases.
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PMID:[Evolution and ecological changes of animal viruses]. 140 23

Isolation of Coxiella Burnetii in the standard laboratory setting is hazardous; therefore most diagnoses are based on retrospective detection of a rising antibody titer to C. burnetti. As a result, this disease is usually undiagnosed or misdiagnosed. Methods for the rapid detection of C. burnetti have now been developed that utilize specific hybridization of labeled DNA probes to nucleic acid in clinical samples. One method detects the presence of C. burnetii 16S ribosomal RNA (rRNA); another uses plasmid sequences. We have developed a probe that detects C. burnetii and one that differentiates between Coxiella strains capable of causing chronic disease and those that cause the acute form. Using these probes, C. burnetii can be identified in blood, urine, and tissue samples. The plasmid-derived probes detect as few as 10(4) organisms and less than 1 ng of Coxiella DNA. A third method differentiates between chronic (endocarditis-causing) strains and those that cause acute Q fever. This method uses the polymerase chain reaction (PCR), in which the target regions of DNA are amplified by iterative cycles of Taq I DNA polymerase chain extension to produce up to a 10(6) amplification of the target sequences. When Southern blotting is used in conjunction with PCR, the test detects as few as 2-9 C. burnetti cells.
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PMID:DNA probes for the identification of Coxiella burnetti strains. 237 70

In the present study, we found that oxidized low density lipoprotein, but not low density lipoprotein, down-regulated base excision repair activity in extracts of mouse monocyte cell line PU5-1.8. An enzyme required in this pathway, DNA polymerase beta, was also down-regulated. In contrast, treatment of monocytes with a combination of ascorbate and alpha-tocopherol up-regulated base excision repair activity and expression of DNA polymerase beta. Co-treatment of monocytes with antioxidants plus oxidized low density lipoprotein prevented down-regulation by oxidized low density lipoprotein. Oxidative DNA damage, as measured by 8-hydroxyguanine accumulation in genomic DNA, was found in cells treated with oxidized low density lipoprotein; 8-hydroxyguanine was not found in the cells treated with low density lipoprotein, antioxidants or oxidized low density lipoprotein plus antioxidants. These results establish a linkage between the DNA base excision repair pathway, oxidative DNA damage and oxidized low density lipoprotein treatment in mouse monocytes. Since oxidized low density lipoprotein is implicated in chronic disease conditions such as atherogenesis, these findings facilitate understanding of genetic toxicology mechanisms related to human health and disease.
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PMID:Modulation of base excision repair by low density lipoprotein, oxidized low density lipoprotein and antioxidants in mouse monocytes. 1078 27

A herpesvirus causing a cytopathic effect was isolated from pulmonary fibroblast cultures established from a European badger (Meles meles). A study was undertaken to classify and to assess some in-vitro growth characteristics of this virus. From a panel of 27 mammalian cell lines, in-vitro replication of the badger herpesvirus (BadHV) was only demonstrated with a mink lung cell line, suggesting a high degree of host specificity. Using PCR with degenerate primers, three independent fragments of the BadHV genome were sequenced. The largest of these fragments comprised a 6.2 kb segment including the DNA polymerase and glycoprotein B genes. Phylogenetic analysis of these sequences demonstrated that the BadHV is novel and clearly grouped with members of the Gammaherpesvirinae. In view of the oncogenic and immunosuppressive potential of many related herpesviruses, it is possible that BadHV can impact on existing acute or chronic disease in badgers.
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PMID:Partial characterization of a novel gammaherpesvirus isolated from a European badger (Meles meles). 1202 47

Today HIV-1 infection is recognized as a chronic disease with obligatory lifelong treatment to keep viral titers below detectable levels. The continuous intake of antiretroviral drugs however, leads to severe and even life-threatening side effects, supposedly by the deleterious impact of nucleoside-analogue type compounds on the functioning of the mitochondrial DNA polymerase. For detailed investigation of the yet partially understood underlying mechanisms, the availability of a versatile model system is crucial. We therefore set out to develop the use of Caenorhabditis elegans to study drug induced mitochondrial toxicity. Using a combination of molecular-biological and functional assays, combined with a quantitative analysis of mitochondrial network morphology, we conclude that anti-retroviral drugs with similar working mechanisms can be classified into distinct groups based on their effects on mitochondrial morphology and biochemistry. Additionally we show that mitochondrial toxicity of antiretroviral drugs cannot be exclusively attributed to interference with the mitochondrial DNA polymerase.
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PMID:Caenorhabditis elegans as a Model System for Studying Drug Induced Mitochondrial Toxicity. 2597 Jan 80