HIV Mutation: A Race Against Time

A headstart has been developed in the race against HIV mutation at the Rockefeller University in New York. Seventeen HIV patients were injected in the first human study of 3BNC117, an antibody that proved to reduce HIV levels 300-fold in patients who received 30 mg per kilogram of weight. 3BNC117 works by binding primary sites on the virus’ shell, aptly named CD4 binding sites after the CD4 cells that the HIV attacks then manipulates to make copies of itself. Normally, CD4 or T-cells are a type of white blood cell that triggers the body’s immune response to foreign bodies such as viruses or bacteria. With the 3BNC117 antibody, the site on the virus initially used to take over healthy CD4s is now inhibited by 3BNC117, essentially “neutralizing” the HIV.

If merely inhibiting the CD4 site can stop HIV, then why has antibody therapy with 3BNC117’s yet to be been deemed a permanent cure? The kicker in using any antibody is that virus mutation is a very real problem. Antibodies that should have the same neutralizing effect as 3BNC117’s are in fact produced by the body; however, the time it takes for the body to naturally produce these antibodies is sufficient for the virus to develop resistance. In other words, the race between producing antibodies and mutating viruses makes the creation of antibodies a continuous process. Luckily, the benefit of 3BNC117 lies in its ability to stop not one, not two but 195 of 237 HIV strains at the same time, lowering the number of viruses that can mutate and multiply. At the same time, 3BNC117 will likely be used alongside HIV medications or other neutralizing bodies that will work collectively to delay this virus proliferation and transfiguration, as the virus could easily cultivate resistance to a single antibody used alone.

In the long run, this successful human research study could have enormous effects. The process was relatively straightforward: researchers took and cloned 3BNC117’s, which are naturally produced in more than one in ten people infected with HIV, then injected study subjects with varying doses. No side effects were apparent; the control group did not have adverse reactions either. The simplicity of the treatment could pave its way as a vaccine for a person yet to be exposed to HIV, an “emergency” response for someone recently exposed or for infants born to HIV+ mothers, or even as a treatment for those whose HIV has already become resistant to existing medications3. Another potential solution could be finding how to speed up the body’s production of 3BNC117’s, eliminating the need for the injections used in the Rockefeller study. Nevertheless, the study marks an immense breakthrough for HIV/AIDS research, and the possibilities for where the researchers may go next are endless.