Population of HIV-targeted CD8 cells fluctuates with viral load during chronic infection

The population of HIV-specific CD8 T cells declines with extended use of effective antiretroviral therapies in infected patients. However, CD8 T cells are remobilised during viral rebound as a result of treatment interruption or failure, according to a report in the August 1st issue of the Journal of Immunology.

“Such dynamics of virus-specific CD8 T cells should be taken into account when elaborating future strategies of scheduled antiretroviral treatment interruptions aiming at restoring specific defenses against HIV,” Dr Brigitte Autran, of the Centre National de la Recherche Scientifique, Paris, France, and members of the RESTIM and COMET study groups, conclude.

The researchers evaluated the association between viral load and HIV-specific CD8 cell populations in 15 chronically infected patients receiving highly active antiretroviral therapy. They were able to monitor the existence of 16 different cytotoxic T-cell epitopes in 14 of the patients.

During the first month of treatment, viral load decreased rapidly. At the same time, the population of HIV-specific CD8 cells in the peripheral blood tripled, while 8 new HIV-specific epitopes, as well as previously undetectable cytomegalovirus-specific epitopes, appeared.

With extended suppression of viral load, the population of HIV-specific CD8 cells in the patients declined, Dr Autran’s group found. But these cells remain capable of remobilisation, as “rebounds of HIV replication are paralleled by peaks in memory CD8 T lymphocytes that quickly restore the pre-existing host-virus quasi-equilibrium,” they write.

Specifically, the authors observed 4 patterns of epitope-specific CD8 cell dynamics during viral rebound: “peaks or disappearance of pre-existing specificities, emergence of new specificities or lack of changes.”

Dr Autran’s group concludes that these dynamics may have an impact on therapeutic interruption strategies aimed at increasing the host response to HIV.


J Immunol. 2000;165:1692-1704.

Source: Reuters Health

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