A soluble form of intercellular adhesion molecule-1 inhibits rhinovirus infection

Article Abstract:

Rhinoviruses, which are small RNA viruses, are responsible for about half of all colds. Most of these viruses attach to cells via a particular molecule called the intercellular adhesion molecule-1 (ICAM-1). In its normal state, the ICAM-1 molecule has five domains that resemble antibody domains, which are located on the outside of the cell. An additional, hydrophobic, domain crosses the cell membrane, where a small cytoplasmic domain on the inside completes the molecule. Using techniques of molecular biology, it is possible to clone most, but not all of the ICAM-1 molecule. Leaving off the hydrophobic and cytoplasmic domains renders the molecule freely soluble, in contrast to the native molecule. This freely soluble molecule retains the domains which the rhinovirus binds to. In tissue culture it is possible to directly observe the destruction of human cells due to infection with rhinoviruses. When this in vitro assay is performed in the presence of soluble ICAM-1, the virus's ability to destroy cells is inhibited, and this inhibition is almost complete at ICAM concentrations of 5 micrograms per milliliter. The inhibition apparently works because all of the molecules on the virus which would normally be available for binding to ICAM-1 on the cell surface are swamped with soluble ICAM-1 before they have an opportunity. The soluble ICAM-1 might serve as an antiviral drug, and would have the advantage of stopping the virus before it infects a cell, rather than trying to cure the infection, as most other agents do. (Consumer Summary produced by Reliance Medical Information, Inc.)

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Nosing ahead in the cold war

Article Abstract:

The majority of antiviral drugs, substances like alpha-interferon, acyclovir, and AZT, act by inhibiting some aspect of viral reproduction after the virus has already penetrated its host cell. New research, however, is beginning to examine the methods by which different viruses adhere to the cell surface, a necessary prerequisite to infection. The discovery that the cell-surface molecule CD4 is the site of attachment for the human immunodeficiency virus has prompted the use of soluble CD4 in the treatment of AIDS. Recent research has now identified the cell surface receptor for the rhinoviruses, those all-too-common agents of the common cold. The receptor, called ICAM-1, for intercellular adhesion molecule-1, can be produced in large quantities by the techniques of molecular biology, and can block the attachment of the viruses to host cells. Does this mean a cure for colds is soon to be available? There are, unfortunately many problems. The cloned soluble ICAM-1 is a protein, and may itself induce an allergic reaction. Antibodies against ICAM-1 may result, and the potential effects of these are not known. It is also not known if the virus will find other routes of infection if ICAM-1 is taken away. Although the study of virus receptors is not likely to produce a quick cure for the common cold, the new knowledge of virology will probably provide an opportunity to devise a new approach to the design of anti-viral drugs. (Consumer Summary produced by Reliance Medical Information, Inc.)

editorial

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Antigenic oscillations and shifting immunodominance in HIV-1 infections

Article Abstract:

A mathematical model for the intercalation among cytotoxic T lymphocytes (CTL) and multiple epitopes of a genetically variable pathogen explains that the CTL response is aimed against conserved epitopes. A supreme response is generated against a single epitope by an antigenically homogeneous pathogen population but complex fluctuating responses are induced against multiple epitopes by a heterogeneous pathogen population. The model predicts that disease progression in an HIV-infected person would be slowed if fighting a single epitope and faster if the virus becomes diverse through evolution.

Physiological aspects, HIV infection, HIV infections, Mathematical models, T cells, Antigenic determinants

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