



An old addage teaches us that, "You learn something new everyday." Such is true after reading this article... I learned that the Human Immunodeficiency Virus (HIV) evolves to escape the immune system, similar to the way bateria mutates under pressure by antibiotics. And, our headlines, both local and international, tell us that HIV is one of the fastest-evolving entities known. Which explains why no one has yet been able to develop a vaccine. The virus mutates so rapidly that what works today in one person may not work tomorrow or in others.
A study published Wednesday in the journal Nature confirms that dizzying pace of evolution on a global scale.
Researchers at the Ragon Institute, at Massachusetts General Hospital in Boston looked at HIV genetic sequences in the United Kingdom, South Africa, Botswana, Australia, Canada and Japan to see how they evolved in response to a key set of molecules in the human immune system, called human leukocyte antigens. These molecules direct the immune system to recognize and kill HIV and other infectious diseases. Genes that encode human leukocyte antigens vary among humans, and even small differences can dramatically affect a person's response to HIV infection.
The study published online Wednesday found that mutations occurred not just in individuals but on a population level. That is, if a particular genetic immune sequence was common in a population, the HIV mutation that evolved to escape it became the most common strain of HIV, even in those without that particular human leukocyte antigen gene.
"What this study does is give an explanation for why there are different HIV strains in different parts of the world," said Dr. Bruce Walker, one of the researchers and director of the Ragon Institute. "The genetic makeup of people in different regions is influencing the virus in specific ways."
This would appear to be bad news for the director of the Ragon Institute of MGH, MIT and Harvard, which was founded to develop vaccines for HIV and other infectious diseases. But Walker saw the results as hopeful. He said that mutations can actually make the virus less fit -- that is, unable to replicate as quickly or do as much damage. His challenge is to find what kind of pressure results in this kind of mutation.
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