Vaccine and antiviral strategies against infections caused by human immunodeficiency virus
1988
Human immunodeficiency virus type 1 (HIV-1) has been clearly associated with a variety of new illnesses, including profound immunodeficiency (acquired immune deficiency syndrome [AIDS]), wasting syndromes (formerly termed AIDS-related complex [ARC]) and neurologic syndromes, including neuropathy, myelopathy and encephalopathy (often termed subacute encephalitis or AIDS dementia complex). HIV-1 preferentially infects T lymphocytes by binding to a membrane receptor protein, CD4, associated with helper function. The virus can also attack macrophages and, possibly, other cells such as neuronal cells, colonic epithelial cells and B lymphocytes. Infection of macrophages or monocytes may be involved in neurologic disease. Knowledge about HIV-1 has rapidly increased, and investigators have characterized its structure, ways in which it infects cells, replicates and is cytopathic for certain cells, and how the immune system responds to it. The ideal vaccine would prevent adsorption of the virus into the cell, but it is difficult to develop stable resistance because the virus has many antigenic patterns and mutates frequently. The results of vaccine trials in animals have not been promising, but work is being done with monoclonal antibodies. Antiviral therapies being investigated include those to prevent virus binding and entry, to inhibit reverse transcription, to inhibit the virus9s life cycle and to restore immune competence in immunocompromised patients.
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