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Researchers believe that macrophage cells in the liver that harbor such inert HIV are not a part of the viral reservoir.
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.
Today, with better understanding of the complex task at hand, cure researchers are investigating multiple avenues and taking the long view.
A recent study found that agents used to wake up resting HIV-infected cells probably work only on 5 percent of such cells.
According to a pair of recent studies, meth was associated with certain HIV-related genetic and immune changes.
Researchers say CD32 is not a biomarker for immune cells latently infected with HIV but one for actively infected cells.
Highlights from HIV and hepatitis C research presented at the 2018 Conference on Retroviruses and Opportunistic Infections (CROI) in Boston
Continuously providing such infants with antiretrovirals as early as possible limits the size of the reservoir.
Researchers will genetically engineer participants’ CD4 cells, disabling the attachment of the virus.
This NIH study closely monitored 10 people with HIV who stopped antiretroviral treatment for weeks to months in a larger cure study.
My headline is, of course, a gross exaggeration. But does this news mean we should hope we get cancer?
In the HIV cure research effort, finding ways to reduce the hidden stores of the virus is key.
Scientists reached this finding thanks to a highly precise means of sequencing HIV’s genetics.
Gilead Sciences’ second round of cure grants supports these five research projects.
This Ohio researcher will be using CRISPR gene editing to target HIV, thanks to funding from The Campbell Foundation.
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