The cells responsible for the second phase decay of HIV-1 viremia following the initiation of antiretroviral therapy have yet to be identified. A dynamic model that considers where drugs act in the virus life cycle places constraints on candidate cell types. In this regard, the rapid drop in viremia in patients starting regimens containing the integrase inhibitor raltegravir is of particular interest. We show here that the time delay between reverse transcription and integration is short in differentiated macrophages, making these cells poor candidates for the second phase compartment under the assumptions of standard models of viral dynamics.
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