After a break in antiretroviral drug therapy in HIV-positive patients, the virus rebounds and begins to multiply. While this was feared to destroy, perhaps irreversibly, patient HIV-specific CD4+ T cells that are preferentially infected by the virus, it has now be shown to actually boost HIV-specific T cell production and activation, thereby boosting the immune response to the virus.
Scheduled interruption and resumption of antiretroviral treatment of HIV-positive patients has generated hopes of reducing drug toxicities, costs, and total treatment time. However there has been concern regarding how this on and off cycling of drug therapy effects viral replication and the patient's ongoing immune response to viral infection. While it was implied that even at high viral loads a small population of these HIV-specific CD4+ T cells remained, they have been difficult to quantify.
Rodney Phillips and colleagues from the University of Oxford developed a highly sensitive technique to visualize, quantify, and track the HIV-specific CD4+ T cell population in patients with early-stage HIV infection who were given a short, fixed course of antiretroviral therapy. They found that return of viral replication after cessation of treatment does not destroy this important T cell population – their numbers were in fact comparable to the numbers observed during therapy. Furthermore, the turnover of these virus-specific cells was increased and the CD4+ T cells were prompted to mature into what are known as effector cells, capable of exerting an immune function that helps coordinate other cells of the immune system to eliminate the virus.
The study will appear online on January 20 in advance of print publication in the February 1 edition of the Journal of Clinical Investigation.
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