Protein HIV Used to Hijack Human Genes
Four years ago, it was estimated that 1.2 million people living in the United States had HIV. Add to that an average of 50,000 new cases per year, and the results are staggering. As the disease progresses into AIDS, the outlook is bleak. One estimate put the number of patients with the advanced stages of HIV at over 26,000. While it is true that therapy can give a person who is HIV-positive a promising future, these treatments are lifelong, and the effects of the infection still manifest themselves in different ways as a patient ages.
A Protein Called Tat
In order to better understand how this wily virus is able to get such a strong hold on its host, experts meticulously performed experiments and studies. The results have brought to light how HIV uses a tiny protein, called Tat, to shut down certain human genes. HIV (a retrovirus) does not have many of its own genes, which is why it searches out and eventually takes over a host cell’s genes. Here is where the small protein, Tat, comes in. Once the command center of the cell has been overtaken, Tat manipulates the genes in order to create a more appealing environment for the virus. Studies show that nearly 400 human genes bind with Tat—and then shut down. When the scientists compared the symptoms of an HIV infection to the genes that were shut down, the two were compatible.
What this tiny protein is able to accomplish is astounding. It does provide useful knowledge that could be applied to halt infection and keep the disease from progressing to AIDS. One European country has already begun working on a vaccine which inhibits Tat in order to try and stop HIV. The results have been promising. However, it will take some more time for anything concrete to be established. In the meantime, more information is being gathered and used to come up with even more effective ways to treat, prevent, and hopefully completely eradicate HIV in the future.
This entry was posted by ADMIN on March 28, 2016 at 4:30 pm, and is filed under HIV, HIV Research. Follow any responses to this post through RSS 2.0.Both comments and pings are currently closed.