HIV researchers at The University of Texas Medical School at Houston believe they have uncovered the Achilles heel in the armour of the virus that continues to kill millions.

The weak spot is hidden in a protein in the virus’s envelope that is essential for HIV to attach to host cells, which then initiates infection and eventually leads to Acquired Immunodeficiency Syndrome or AIDS.

Normally the body’s immune defences can ward off viruses by making proteins called antibodies that bind the virus. However, HIV is a constantly changing and mutating virus, and the antibodies produced after infection do not control its progression to AIDS.

The newly discovered ‘Achilles heel’, a tiny stretch of amino acids in the protein, is now under study as a target for therapeutic intervention.

Sudhir Paul, Ph.D., pathology professor in the UT Medical School, said, “HIV needs at least one region that must remain constant to attach to cells. If this region changes, HIV cannot infect cells.”

“HIV uses the same constant cellular attachment site to silence antibody producing cells. The result is that the body is fooled into making abundant antibodies to the changeable regions of HIV but not to its cellular attachment site. HIV’s cleverness is unmatched. No other virus uses this trick to evade the body’s defences,” he explained.

Paul’s group has engineered antibodies with enzymatic activity, also known as abzymes, which can attack the Achilles heel of the virus in a precise way.

Unlike regular antibodies, abzymes degrade the virus permanently. A single abzyme molecule inactivates thousands of virus particles. Regular antibodies inactivate only one virus particle, and their anti-viral HIV effect is weaker.

“The abzymes recognise essentially all of the diverse HIV forms found across the world. This solves the problem of HIV changeability. The next step is to confirm our theory in human clinical trials,” Paul said.

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