Selective alterations in immunoregulatory lymphocyte subsets in early HIV (human T-lymphotropic virus type III/lymphadenopathy-associated virus) infection

In order to characterize the effects of HIV (human T-lymphotropic virus type III/lymphadenopathy-associated virus) on the immune system, Leu8- and Leu8+ subsets of CD4 and CD8 cells were studied in seropositive homosexually active men without acquired immune deficiency syndrome (AIDS). Controls incl...

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Veröffentlicht in:Journal of clinical immunology 1987-03, Vol.7 (2), p.140-150
Hauptverfasser: GIORGI, J. V, NISHANIAN, P. G, SCHMID, I, HULTIN, L. E, HUEI-LING CHENG, DETELS, R
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Sprache:eng
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Zusammenfassung:In order to characterize the effects of HIV (human T-lymphotropic virus type III/lymphadenopathy-associated virus) on the immune system, Leu8- and Leu8+ subsets of CD4 and CD8 cells were studied in seropositive homosexually active men without acquired immune deficiency syndrome (AIDS). Controls included both heterosexual men and HIV-seronegative homosexually active men. The decrease in CD4 levels, observed in HIV-seropositive men who were asymptomatic, as well as in those who had persistent generalized lymphadenopathy or constitutional symptoms of HIV infection, occurred proportionally in both the Leu8- and the Leu8+ CD4 subsets. This observation, that HIV infection does not selectively diminish either subset of CD4 cells, indicates that the selective loss of T cell-mediated functions which accompanies the development of AIDS is not related to preferential loss of the Leu8+ CD4 subset. Among CD8 cells, however, HIV infection resulted in a threefold elevation in the number of Leu8- CD8 cells, while the number of Leu8+ CD8 cells remained constant. The increase in Leu8- CD8 cells was present in recent seroconverters, persistently seropositive men, and patients with AIDS. We propose that the increase in Leu8- CD8 cells represents an HIV-specific cytotoxic T-cell response. These cells may operate by killing infected CD4 cells, thereby partially controlling viral infection while simultaneously contributing to the destruction of the immune system.
ISSN:0271-9142
1573-2592
DOI:10.1007/BF00916008