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BYU study shows how Alpha-1 protein prevents HIV virus from multiplying
Deseret News
PROVO — A set of twins, a failed vaccine and a protein “stop sign” have led three research teams conducting different studies at Brigham Young University (BYU) to increased understanding of how HIV changes and produces more virus.
One of the BYU studies showed how the alpha-1 antitrypsin protein prevents the HIV virus from multiplying.
A number of years ago, identical twin baby boys received a tainted transfusion and both became HIV-positive. Now, one of the twins has a near-normal immune system and pretty good health, while the other boy is five years behind him on the growth chart and has experienced a number of complications.
That provocative difference became the foundation of one of the three studies, as researchers led by Brigham Young University biology department chairman Keith Crandall studied how the virus changed in each twin. They were joined in the study by scientists at the National Cancer Institute.
The second study focused on an HIV vaccine Thailand was trying to develop that didn’t prove effective. What Crandall and other researchers found there, though, was a population that had been subjected to regular blood draws, including some before and after they contracted HIV. Those samples afforded the researchers another look into how the virus evolved.
The third study, by the Department of Chemistry and Biochemistry chairman Greg Burton, colleagues from BYU and the University of Colorado Health Sciences and student Xueyuan Zhou, confirmed an earlier report that a naturally occurring protein prevents HIV from multiplying. But unlike that earlier research, they were also able to explain how the protein works, not just what happens.
Burton said the study that looked at the effect of the protein a-1-antitrypsin was a follow up to earlier research that found the protein could inhibit HIV. AAT, as the protein is called, has already been approved for use in treating chronic obstructive pulmonary disease. The scientists explained that “at the right levels, AAT alters the activation of a separate protein that HIV needs to transcribe its genetic code in the replication process. Without the needed protein, HIV doesn’t produce more virus.”
“The importance of this study is that we moved ahead from earlier research. The effect was known, but we showed the mechanism,” he said.
