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Any HIV cure on the horizon will have to tackle macrophage immune cells as well as CD4 T Cells, a study indicates.
One avenue in the HIV cure research field involves using agents that prevent reactivation of HIV replication in latently infected cells.
In a study of people with a low but detectable viral load despite adherence to treatment, infected cells were apparently cloning themselves.
Today, with better understanding of the complex task at hand, cure researchers are investigating multiple avenues and taking the long view.
As a result, cure treatments may have to approach these two targets differently.
Such latently infected cells remain under the radar of antiretroviral treatment, which only works on replicating cells.
A recent study found that agents used to wake up resting HIV-infected cells probably work only on 5 percent of such cells.
Researchers say CD32 is not a biomarker for immune cells latently infected with HIV but one for actively infected cells.
Gilead Sciences’ second round of cure grants supports these five research projects.
Campbell Foundation funds nontraditional avenues of research.
The anti-alcoholism drug Antabuse (disulfiram) apparently prompts the activation of cells latently infected with HIV.
Scientists have created a two-headed protein that awakens latently HIV-infected immune cells and summons an immune response to kill them.
A so-called TLR7 agonist has shown promise in its ability to wake infected cells from a dormant state and cause them to produce HIV.
The virus itself, and not infected immune cells, controls when replication stops and starts.
The HIV viral reservoir may be as much as 60 times larger than scientists have initially estimated, posing a setback for cure research progres...
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