Scientists have long held the prevailing view that during HIV infection the depletion of T cells is the result of direct HIV virus–mediated killing. In the September 15 issue of the Journal of Clinical Investigation, Marc Hellerstein and colleagues at the University of California in Berkeley report that it is the chronic activation of the host immune system in response to HIV infection that primarily contributes to T cell loss.
A series of influential studies published in the mid-1990s described the rapid decay of viral load following administration of highly active antiretroviral therapy (HAART), and proposed that HIV infection was associated with a high rate of virus turnover and short lifespan of infected cells. This suggested that HIV infection of susceptible CD4+ T cells led to such high rates of cell death, that compensatory T cell proliferation was inadequate to maintain sufficient T cell numbers and therefore compromised the ability of the immune system to fight the virus.
This view was recently challenged by observations that not only were virus-infected cells dying, but a greater number of uninfected bystander T cells underwent programmed cell death that was not a direct result of HIV infection. Therefore, a new theory has been proposed in which high levels of T cell proliferation reflects a state of chronic immune activation following HIV infection as opposed to simple compensatory proliferation.
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Researchers from the Institute for Quantum Computing (IQC) at the University of Waterloo led the development of a new extensible wiring technique capable of controlling superconducting quantum bits, representing a significant step towards to the realization of a scalable quantum computer.
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14.10.2016 | Event News
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