Abstract

PIP: Recent research suggests that the collapse of the immune system that accompanies acquired immunodeficiency syndrome (AIDS) stems largely from a single defect: a reduction in the number and a change in the function of the T4 lymphocytes. This knowledge may make it possible to lessen the effects of AIDS, and eventually to prevent and cure it. The loss of T4 lymphocytes from the blood, lymph nodes, spleen, and other tissues in which they are normally concentrated is a consistent finding in AIDS patients. Without the help of T4 cells, B cells are unable to produce adequate quantities of antibody to the AIDS virus or to any other infection. Infected T4 cells are also the source of soluble suppressor factor, which blocks T-cell-dependent immune responses. The drug suramin has been found to be capable of preventing the AIDS virus from infecting and damaging T cells in vitro. Other drugs that counteract reverse transcriptase or interfere with later stages in the viral life cycle may also prove useful. Under investigation are antiviral drugs that have the added effect of stimulating the host's immune system. These drugs seem to work by inhibiting enzymes that are crucial to the synthesis of viral RNA and DNA. The genetic variability of the AIDS virus complicates vaccine development, although it may be possible to identify invariant regions of the viral envelope to which antibody can bind effectively. The genome of the AIDS virus has been found to contain a sequence known as tat, which encodes a similar regulatory protein. If the AIDS virus could be modified genetically by deletion of tat or the sequence with which the tat protein interacts, it could serve as a safe vaccine.