Role of abortive retroviral infection of neurons in the spongiform CNS degeneration

Article Abstract:

Retroviruses cause infections, such as AIDS, which can have adverse neurological effects. It is not certain if the neurological damage that retroviruses cause is due to a direct or indirect effect of the virus on the nerve cells. The mouse retrovirus Cas-BR-E causes a neurological disease affecting the lower motor neurons causing spongiform (resembling a sponge) degeneration of the neurons in the brain and spinal cord. The virus is known to enter the central nervous system (CNS) by the blood and is found in the endothelial cells, which line the interior walls of blood vessels. The virus was found in the neurons, indicating that the virus has a direct effect on the neurons. The envelope protein of the virus, which is part of surface of the virus and is usually present in infected cells, was not detectable in the neurons, but was present in non-neuronal tissue. The gene encoding the envelope protein is translated to messenger RNA in CNS tissue, one of the steps that is necessary for the expression of the envelope protein. This indicates that a step further in the process of protein expression is impaired, which would stop the virus from maturing and further dividing. The disease, then, may be the result of the incomplete replication of the virus inside the neurons. These results may explain why when neurons were examined for the presence of the envelope protein in various diseases with neurological symptoms such as AIDS, adult T cell leukemia, and noninflammatory neurodegenerative diseases such as Alzheimer's and Creutzfeldt-Jakob disease, the virus was not found. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models, Physiological aspects, Central nervous system diseases, Neurons, Retrovirus infections

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Long-range cis effects of ectopic X-inactivation centres on a mouse autosome

Article Abstract:

X chromosomes in mammals can generate complete inactivation to compensate for gene dosage differences between two-X-chromosomed females and single-X-chromosomed males. Transcriptional silencing of one female X chromosome is controlled in cis by Xist(supra 2), whose ribonucleic acid (RNA) product coats the inactive X chromosome and the X-inactivation center (Xic (supra 4)). A study found that ectopic Xist RNA completely coats transgenic chromosome 12. Ectopic Xic action resulted in the delay of the replication of the deoxyribonucleic acid and the hypoacetylation of histone H4.

X chromosome, Dosage compensation (Genetics)

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DNA hypomethylation leads to elevated mutation rates

Article Abstract:

Evidence for genome wide demethylation as a step in carcinogenesis comes from frequently observed global DNA hypomethylation in tumour cells. DNA hypomethylation has also been linked to abnormal chromosomal structures. It is reported murine embryonic stem cells nullizygous for the major DNA methyltransferase gene, showed significantly higher mutation rates at the endogenous hypoxanthine phosphoribosyltransferase gene and the integrated viral thymidine kinase transgene.

DNA, Carcinogenesis, Methylation

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