Important note: Information in this article was accurate in 1999. The state of the art may have changed since the publication date.
Important note: Information in this article was accurate in 1999. The state of the art may have changed since the publication date.
Reuters NewMedia - Thursday August 19, 1999
Patricia Reaney
HIV infects the body through receptors for chemokines -- signaling chemicals that activate specific types of white blood cells in the immune system to protect the body against invaders.
HIV mainly uses receptors, or chemical doorways, that protrude from white blood cells on the CCR5 and CXCR4 chemokines.
Carlos Martinez-A (Eds: correct) and a team of immunologists at the Universidad Autonoma de Madrid have shown how a mutant receptor for another chemokine called CCR2, which is not used by the HIV virus to invade cells, increases resistance to the disease by blocking entry through the CCR5 and CXCR4 receptors.
"It opens up a new path to screen for new drugs to fight HIV," Martinez-A said in a telephone interview.
The mutant CCR2 receptor acts like a key that closes the main doors and prevents the virus from entering healthy cells.
The most potent anti-AIDS drugs either block the protease enzyme and prevent HIV-infected cells from maturing or stop the replication of the virus. "This will open up a third way. It might be very interesting in itself or could be used in collaboration with the other two to prevent or delay AIDS development in people infected with HIV," Martinez-A said.
Scientists knew that AIDS took longer to develop in people with the mutant CCR2 receptor but did not know why.
Martinez-A and his team, whose research is published in the latest issue of the journal Nature, have solved the puzzle.
"This receptor is able to associate with the receptors that are used by the virus to infect cells. In doing so it blocks the ability of the other receptors to be used by the virus," said Martinez-A.
The HIV virus will still try to find other chemokine receptors, but because these two are the most important ones, the disease is delayed.
AIDS usually develops two to four years later than normal in HIV-infected people with the mutated receptor.
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