This so-called biomarker could aid in cure treatments by guiding efforts to drain the viral reservoir.
Because standard antiretroviral (ARV) treatment for HIV works only when a cell is active and replicating, latent cells essentially hide from treatment. But the cells may reactivate at any time and send the viral load shooting up if ARVs are discontinued or become less effective because of drug resistance or poor adherence to a daily regimen. The existence of such latently infected cells is one of the main reasons curing the virus is so extremely difficult.
Publishing their findings in the journal Nature, researchers built on their newly discovered means of generating a large population of latently infected immune cells without activating them into a replicating state. Next, in a laboratory experiment, they examined differences in the expression of human genes in the context of such latently infected cells compared with uninfected cells.
Their research zeroed in on one gene called FCGR2A, which encodes a protein called CD32a that operates as a receptor for a portion of antibodies known as immunoglobulin G, or IgG. The researchers subsequently found that CD32a is expressed on the surface of latently infected immune cells but not on replicating infected cells or uninfected cells.
Further studies could use CD32a as a target to identify latently infected cells in an attempt to drain the viral reservoir. However, since this biomarker is expressed on only about half of latently infected cells, questions remain about how treatments could efficiently identify the other set of latently infected cells.
Also, targeting CD32a could interfere with important natural processes for other cells that make use of the protein. Additionally, the researchers looked only at CD4 cells found in the blood, which represent just about 2 percent of the body’s CD4 cells. So it’s unclear whether this marker would identify CD4s elsewhere in the body, such as in the lymph nodes.
To read the MedPage Today article, click here.
To read the study abstract, click here.
Read more articles from POZ, here.
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