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Lymphotoxin production in AIDS
1Department of Epidemiology and Public Health, Yale University School of Medicine, PO Box 3333, 60 College St, New Haven, CT 06510, USA.
The etiological agent of the acquired immunodeficiency syndrome (AIDS), lymphadenopathy-associated virus/human T-lymphotropic virus III (LAV/HTLV-III), infects the OKT4(+) subset of T cells and causes their death. In this article Nancy Ruddle proposes that the trans acting protein of LAV/HTLV-III kills cells by inducing them to make a cellular cytotoxic protein, lymphotoxin, which in abnormally high quantities results in the cells' self-destruction. Lymphotoxin may even become serum detectable. It may induce immunosuppression and susceptibility to opportunistic infections by organisms such as Pneumocystis carinii. Defects in tumor immunity may result from depletion of OKT4(+) cells.
The etiological agent of the acquired immunodeficiency syndrome (AIDS), lymphadenopathy-associated virus/human T-lymphotropic virus III (LAV/HTLV-III), infects the OKT4(+) subset of T cells and causes their death. In this article Nancy Ruddle proposes that the trans acting protein of LAV/HTLV-III kills cells by inducing them to make a cellular cytotoxic protein, lymphotoxin, which in abnormally high quantities results in the cells' self-destruction. Lymphotoxin may even become serum detectable. It may induce immunosuppression and susceptibility to opportunistic infections by organisms such as Pneumocystis carinii. Defects in tumor immunity may result from depletion of OKT4(+) cells.
