| Autor: |
Spring, M., Stahl-Hennig, C., Stolte, N., Bischofberger, N., Heeney, J., ten Haaft, P., Tenner-Ra`cz, K., Ra`cz, P., Lorenzen, D., Hunsmann, G., Dittmer, U. |
| Zdroj: |
Virology; January 5, 2001, Vol. 279 Issue: 1 p221-232, 12p |
| Abstrakt: |
Losing the decisive virus-specific functions of both CD4+ and CD8+ T lymphocytes in the first weeks after immunodeficiency virus infection ultimately leads to AIDS. The SIV/rhesus monkey model for AIDS was used to demonstrate that a 4-week chemotherapeutic reduction of viral load during acute SIV infection of macaques allowed the development of a competent immune response able to control virus replication after discontinuation of treatment in two of five monkeys. Increasing SIV-specific CD4+ T-helper-cell proliferation was found in all macaques several weeks after treatment, independent of their viral load. However, only macaques with low viral loads showed persistent T-cell reactivity of lymph node cells. In contrast to animals with higher viral loads, T-helper-cell counts and memory T-helper cells did not decline in the two macaques controlling viral replication. Lymphocyte apoptosis was consistently low in all treated macaques. In contrast, high CD8+ lymphocyte death but only slightly increased CD4+ lymphocyte apoptosis were observed during the first weeks after infection in untreated control animals, indicating that early apoptotic death of virus-specific CTL could be an important factor for disease development. Antiretroviral treatment early after infection obviously retained virus-specific and competent T lymphocytes, whereby a virus-specific immune response could develop in two animals able to control the viral replication after cessation of treatment. |
| Databáze: |
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