 | Figure 2
Nature Medicine
9, 853 - 860 (2003)
doi:10.1038/nm0703-853
HIV-1 pathogenesisMario Stevenson | | | | Figure 2. An overview of viral reservoirs and their relative contribution to plasma viremia.
Steady-state levels of plasma viral RNA reflect the cumulative production of virus from the various cellular reservoirs and the turnover of virus-producing cells in those reservoirs. When viral replication is inhibited by HAART, plasma viral RNA decays in four distinct phases, suggesting that the various viral reservoirs are turned over to very different extents as a result of HIV-1 infection. The first phase reflects virus produced predominantly from activated CD4+ T cells. In the second phase, macrophages may be the main source of virus, because the decay characteristics of plasma viremia in this phase approximates the lifespan of the tissue macrophage. Resting (G1) T cells may also contribute to this more slowly turning over reservoir. The third phase reflects an extremely low and chronic production of virus from a stable reservoir. Presumably cells constituting this reservoir maintain a low and sustained output of virus, while simultaneously resisting cytopathic effects and killing by cytotoxic T lymphocytes. Resting CD4+ T cells or DCs may be the sources of virus in this covert reservoir. The fourth phase of decay is based on in vitro measurements of the frequency of latently infected CD4+ T cells, but FDCs harboring trapped virions might also be a long-lived source of infectious virus in this phase.
Katie Ris |
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