HIV susceptibility conferred to human fibroblasts by cytomegalovirus-induced Fc receptor
Article Abstract:
Before a virus can infect a cell, it must attach to it. Some viruses attach to virtually all cells, and successful infection is determined by other factors. The human immunodeficiency virus (HIV), however, is apparently quite fastidious, and attaches directly only to cells which express the CD4 antigen. This fact is of some clinical interest; antibodies to CD4 will block the virus from attaching. Some clinical trials are being conducted using excess free CD4 to let any free viruses find some antigen to attach to, before they find a target cell. Under some conditions, HIV can successfully bind to cells which do not express CD4. Certain cells, such as macrophages, express an Fc receptor, which binds the Fc region on an antibody molecule. Under normal conditions this would enable the macrophage to engulf antibody-covered bacteria or the like. However, if HIV is covered with antibody molecules, it can attach to the Fc receptor as well, and capitalize on this attachment to infect the cell. The antibodies, designed for protection, ironically participate in the spread of the virus. Investigators have now demonstrated that successful HIV infection of human fibroblasts may occur with the help of another virus, the cytomegalovirus. Fibroblasts, which are ubiquitous in the body, are not normally susceptible to HIV infection. However, in vitro experiments have shown that after cytomegalovirus infection, the fibroblast cells can bind the Fc portion of the antibodies. An HIV particle, covered with antibodies, may now gain access to the fibroblast. It may also be possible that some of the viral machinery set up by the cytomegalovirus may help to spread HIV, but this has not yet been demonstrated. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1990
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Spoilt for choice of co-receptors
Article Abstract:
The human and simian immunodeficiency viruses (HIV,SIV) attach and gain entry to cells through surface glycoproteins, binding efficiently to the CD4 cell-surface receptor of T lymphocytes. Different co-receptors are used to trigger viral entry. Further co-receptors for SIV and HIV infection have been discovered and more work is now needed to determine the contribution of each to HIV infection and pathology.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1997
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A finger on the culprit
Article Abstract:
The recent discovery of an unknown human herpes virus in Kaposi's sarcoma (KS) has encouraged research on the early stages of tumor formation. The role of the virus is unclear, but this new virus acts along with HIV to promote the growth of HIV lesions in AIDS-infected KS patients. This new virus could be a sexually transmitted virus that is expressed in HIV-positive gay men.
Publication Name: Nature
Subject: Zoology and wildlife conservation
ISSN: 0028-0836
Year: 1995
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