A New HIV strategy

Don't work harder, work smarter. This saying is frequently applied in business, schools, and now possibly in science? HIV researchers are testing new ways to make a more effective HIV treatment.
           HIV has proven to be one of the trickiest human diseases to treat due to a variety of reasons. For one, it specifically kills immune cells, which eventually allows opportunistic pathogens to infect and kill AIDS patients. More problematically, HIV mutates extremely fast. Mutations are generally thought of as a bad thing, as they are errors in the DNA. However, for HIV having such a high mutation rate is a great thing, because it allows it to change faster than the immune system can recognize and kill it. The high mutation rate is favored, because the immune system will weed out any viral particles that don't mutate and retain the old, "known" form.
           Current HIV treatment options focus on trying to both get the body to recognize and destroy the virus, and to try to prevent mutations in HIV as long as possible by throwing lots of different drugs at it.This is known generally as a drug cocktail, or more recently as HAART (Highly Active Antiretroviral Therapy). HAART combines three different classes of HIV medication, each of which targets a different vital component of the virus. Generally, this regimen includes a nucleoside reverse transcriptase inhibitor, a protease inhibitor, and a non-nucleoside inhibitor. Basically, both kinds of the reverse transcriptase inhibitors prevent HIV from copying its genetic material, and the protease inhibitor prevents the complete formation of mature viral proteins. I like to think of this approach as "playing the odds". By targeting more than one component of the virus, HAART increases the number of mutations HIV has to accumulate in order to be successful, which decreases the odds that one HIV viral particle will be able to do so. Now, researchers are proposing a new strategy I like to think of as "go ahead, mutate, we dare you".
           A collaboration between researchers at the Ragon Institute, MIT, and Harvard have identified regions of HIV that decrease its fitness when mutated. Basically, if the virus tries to mutate these regions to escape detection by the immune system, it will be unable to survive. If it doesn't mutate these regions, the body will be able to recognize and destroy it. It's rather like being caught between a rock and a hard place for HIV.
           While these results were discovered using computer algorithms, more details of which can be found here, the researchers strengthened their findings by comparing to real human data. They found that patients who control HIV on their own without medicine have T cells that target these same regions on HIV, and that strains with mutations in these regions of the virus are extremely rare in nature, indicating that there is strong selection working against such strains. Additionally, because this amino acid sequence is so highly conserved, there's potential for a vaccine to be developed with these regions. Right now, HIV mutates too fast for a vaccine to ever be effective.
           Personally, I find this study fascinating because it takes a whole new approach to the HIV problem. Instead of trying to circumvent the problem of HIV's high mutation rate, they are using its mutation rate against it. It is a novel idea, and from my very non-expert point of view, one with a good chance of success.