HIV is very elusive and devastating retrovirus. First globally recognized as a problem in the 1980’s, physicians worldwide have been trying to figure out and find a cure/vaccine to this virus, but unfortunately to no prevail. Part of the problem is that the cells that they infect and stay undetected in evade the body for a long time until it is too late. These cells are called T-cells which are a type of lymphocyte that that plays a central role in cell-mediated immunity.
Scientist are trying to find these elusive cells, study and then ultimately kill them. The good news is that recently, scientist may actually be on to making more progress with this disease. On an infected T-cell that is dormant, there is a receptor called CD32a that is a protein. With this receptor, the protein provides a way to distinguish these sleeper T cells from other immune-system cells.
The receptor provides hope that scientists could target these silent, infected cells and destroy them. One reason why researchers are interested is because of antiviral drugs. These drugs are good because they prevent the virus from spreading throughout the body, and infected immune cells like the T-cell to stop transcribing and replicating the viral DNA. But because there is a small portion of infected T-cells that are dormant, the drugs nor our immune systems detect these cells.
Then arises the problem if the patient stops taking the drug then these cells can become active and the problem then progresses. In 2012, HIV researchers found and attempted a new approach to targeting dormant, infected T cells. This technique was called “shock and kill”, which essentially means they are reactivating/trying to kickstart viral replication in these dormant T-cells. This may be a big red flag because why would you want to “turn on” these infected cells.
But actually it is a good idea because with this theoretically then the viral drugs should work and we shouldn’t have to worry as much. Unfortunately for the most part when testing this, the HIV infected cells were not stimulated enough. This is where CD32a comes into play. When using a fluorescent tagger in gene expression between non-infected and infected T-cells, the infected T-cells showed this gene. Therefore scientist believe, by using an antibody that sticks to CD32a, the researchers then pulled cells expressing the protein out of human blood samples from HIV-infected people. Hopefully following this, then the ultimate goal would be to see if CD32a turns out to be a reliable marker, so it can be used to target drugs to the latent T-cells.