Sequence analysis and acute pathogenicity of molecularly cloned SIV

Article Abstract:

The simian immunodeficiency virus (SIV) is regarded as roughly analogous to the human immunodeficiency virus (HIV), which causes AIDS in humans. One of the ways in which the function of a virus and the pathogenesis of disease can be understood, is by the study of mutants. Such study can show how alteration of a particular protein of the virus can produce alterations in the disease process. In the past, obtaining mutants for study was a matter of chance, but today the techniques of molecular biology make it possible to produce the desired mutants almost on demand. The procedure involves cloning the viral genes, selecting mutant genes, and then inserting the genes into an appropriate cell to make mutant virus. Unfortunately, efforts to use this technique for the production of infectious SIV were disappointing until recently. Although virus could be produced, it was not infectious in laboratory monkeys. However, this problem has now been solved, and molecularly cloned SIV has been prepared which is infectious in macaque monkeys. The SIV prepared in this fashion is dramatically pathogenic. Unlike HIV, which produces a slowly developing infection that harms its host indirectly by damaging the immune system, SIV can harm its host directly by causing an acute infection. Since the acute infection is caused by a cloned virus, the effect cannot be the result of some unknown viral contaminant, and may be attributed directly to SIV. Such an infection is unusual for the class of viruses which includes HIV. The class is called lentiviruses, and are named for their traditionally slow action. The molecular cloning of infectious SIV now clears the way for the testing of new SIV clones, each deficient in some particular gene, which should provide a great deal of information about the viral infection and the disease which follows. (Consumer Summary produced by Reliance Medical Information, Inc.)

Development and progression, Simian immunodeficiency virus, Retrovirus infections

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Blocks on the viral exit

Article Abstract:

The current, but largely unsatisfactory, therapy for AIDS is zidovudine, previously called AZT. This compound tries to limit reproduction of the AIDS virus by inhibiting the virus' special enzyme reverse transcriptase. Novel approaches to the treatment of AIDS are likely to attempt to interfere with the virus at other points in its replicative process. One such point is the process by which viral proteins are brought to the cell surface after being produced by the synthetic machinery of the infected host cell. In the June 14, 1990 issue of Nature, Buonocore and Rose describe the development of a mutant CD4 molecule which may serve as an 'intracellular immunization'. CD4 is the molecule on T-cells to which the virus attaches during the first step of infection. Therefore, proteins on the viral envelope clearly stick to CD4 on the cell's surface. When the mutant CD4 gene is introduced into a cell, the CD4 molecule is manufactured, but it cannot be properly transported to the cell surface. If the cell is also infected with the AIDS virus, viral proteins stick to the same mutant CD4 molecule, and are also prevented from reaching the cell's surface. The net effect is to prevent mature virus particles from being assembled from the protein pieces, an event which normally takes place after the protein components are at the cell surface. The idea is elegant, but it is far from certain that the effect will prove to be a useful treatment for HIV infection. Long before this approach nears a clinical trial, other therapies will be evaluated, including one that uses polysulfated polysaccharides to block the binding of the target cells, and another that uses a highly specific inhibitor of the AIDS virus' protease enzyme. (Consumer Summary produced by Reliance Medical Information, Inc.)

Physiological aspects, HIV infection, HIV infections, editorial

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Interference with the assembly of a virus-host transcription complex by peptide competition

Article Abstract:

Infection with the herpes simplex virus can cause blisters on the skin and mucous membranes. One type of herpes simplex virus can result in an infection which occurs in the facial area; another type causes infection in the genital region. For proteins of the herpes simplex virus to be synthesized, a complex of deoxyribose nucleic acid (a cellular factor involved in the synthesis of proteins) and a viral regulatory protein must be formed. If the viral regulatory protein is altered, a compound is formed that interferes with normal protein synthesis. These interfering complexes can be used to inhibit the synthesis of viral proteins, and perhaps inhibit the replication of viruses such as herpes simplex virus and human immunodeficiency virus, which causes acquired immunodeficiency syndrome (AIDS). A peptide (a small sequence of amino acids which are the building blocks of proteins) of the herpes simplex virus regulatory protein was shown to inhibit assembly of the complex. The use of small peptides instead of whole protein is a more feasible approach in developing treatments for inhibiting virus synthesis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Growth, Metabolic regulation, Growth regulators, Antiviral agents, Peptide regulatory factors, Herpes simplex

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