Neutralizing antibodies- bnAbs, eventually arise naturally in about half of HIV-infected people, but they develop too late to be effective, long after the virus has repeatedly mutated and inserted itself into the genome of host cells.
Searching for a way to elicit bnAbs before HIV infection so they can block the virus if they encounter it, a research team led by the Duke Human Vaccine Institute identified an important protein that is highly active in people who develop bnAbs compared to those who don’t.
The protein-RAB11FIP5, appears to be involved in changing the distribution and function of natural-killer cells, which are among the immune system’s early responders during a viral infection. Natural killer cells also play a role in autoimmune diseases, when the body’s immune system turns on itself.
New natural killer cell cargo-carrying pathway that appears to be important in regulating the bnAb production. Researchers analysed the molecular differences between HIV-infected people who make bnAbs, and those who don’t. They identified 239 infected people, and screened them to find approximately 50 on each extreme-those with the highest numbers of bnAbs, and those with the lowest.
Researchers used RNA sequencing analyses to determine the molecular differences that distinguished between those who produce bnAbs and those who do not, finding a marked discrepancy in the RAB11FIP5 gene expression. The data suggest that natural killer cell dysfunction permits bnAb development, implicating Rab11 as a modulator of the HIV antibody response. This can generate better HIV antibody response.
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