Phenotypic mixing between human immunodeficiency virus and vesicular stomatitis virus or herpes simplex virus

Article Abstract:

A great many viruses consist of an outer envelope, which surrounds an inner core. The outer envelope contains proteins which bind to target cells and promote the entry of the virus into the cell, while the core contains the genetic material of the virus and the enzymatic machinery to promote replication of the virus. When a single cell is infected with two viruses, it is sometimes possible to obtain phenotypic mixing. In other words, the genome of one virus may be surrounded by the envelope of another. Such mixing may be more than just a laboratory curiosity. Being surrounded by the envelope of another virus may provide the genes a way to infect cells which are not normally part of their normal host range. Research has now demonstrated, at least in tissue culture, that genes of the human immunodeficiency virus may be surrounded by the envelope of the vesicular stomatitis virus (VSV) or the envelope of herpes simplex virus (HSV). Phenotypically mixed viruses were prepared by infecting the H9 cell line, already infected with HIV, with either VSV or HSV. Investigators were able to demonstrate the existence of phenotypic mixtures by showing that the recovered virus stock could now infect cells which were normally refractory to infection with HIV. That is, cells which can be infected with herpes simplex, for example, were now being infected by the herpes simplex envelope carrying the AIDS virus genes within. Like Greeks climbing from the Trojan horse, the HIV genes could successfully infect the cell once having gotten inside the gates. Although it is uncertain if such an effect actually occurs in human patients infected with HIV, the disturbing possibility remains that the AIDS virus may borrow some phenotypic characteristics from other viruses it encounters and expand its ability to infect both other cells and other people. (Consumer Summary produced by Reliance Medical Information, Inc.)

Phenotype, Phenotypes, Herpes simplex virus

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HIV-1 env sequence variation in brain tissue of patients with AIDS-related neurologic disease

Article Abstract:

Over 60 percent of patients with AIDS develop neurologic disorders because the human immunodeficiency virus type 1 (HIV-1) infects the tissues of the brain. Virus has been isolated from brain tissue and blood cells of patients with AIDS who have neurologic disorders. One of the proteins of the viral isolates, known as gp120, which is present on the outer coat (envelope) of the virus, was genetically analyzed. Viruses that were isolated from the different sites in each patient were found to contain differences in the genes coding for the gp120 molecule. Certain subtypes of the viruses were more prevalent in one anatomical site compared with another. For example, certain subtypes are present in higher frequency in brain tissue compared with blood cells. This suggests that viruses that are closely related but are genetically different can be present in the same individual. This is thought to occur due to genetic changes which occur in the original virus. Other studies have also suggested that the virus is different in the brain and blood. This finding could aid in the understanding of how the virus causes disease symptoms, including disorders of the neurological system. (Consumer Summary produced by Reliance Medical Information, Inc.)

HIV infection, HIV infections, Dementia

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A palindromic element in the human immunodeficiency virus long terminal repeats binds retinoic acid receptors and can confer retinoic acid responsiveness on a heterologous promotor

Article Abstract:

Part of a DNA sequence in the human immunodeficiency virus (HIV) called the long terminal repeat (LTR) appears capable of binding to the retinoic acid receptor. Part of the LTR is called site B, and it is known to be a negative promotor that inhibits HIV synthesis. Site B was artificially synthesized and its ability to bind to the retinoic acid receptor (RAR) was measured. Gel electrophoresis revealed that the site did bind to RAR. Site B was added to a stretch of DNA that turns on a gene for the enzyme chloramphenicol acetyltransferase and the resulting gene was introduced into a cell line. The cell line then became responsive to retinoic acid. However, when an HIV LTR sequence was added to the cell line, the cells were not responsive to retinoic acid. It is possible that other factors present in the virus might make the viral site B responsive to retinoic acid.

Research, Cell receptors

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