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To: Richard Phillips who wrote (4220)	8/18/1999 1:45:00 PM
From: RickV	Respond to of 4891

pops, the doc doesn't speak any language,, just a techy at heart spend money and who cares about the finances..... rick

To: Richard Phillips who wrote (4220)	8/20/1999 8:58:00 PM
From: paper man	Respond to of 4891

ALERT Related subjects: Good... good, this is good. paragraph 2.... lets just swith em off or on. Or, if you would like, in paragraph 3, lets just close the door. me thinks reticulose getting exposure...IMO Study sheds new light on how HIV infects cells By Patricia Reaney LONDON (Reuters) - Spanish researchers have discovered why the progression of the HIV virus that causes AIDS is delayed in some sufferers, which could provide a new approach to fighting the disease. 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. 18:28 08-18-99 Copyright 1999 Reuters Limited. All rights reserved. Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon

To: Richard Phillips who wrote (4220)	8/20/1999 9:20:00 PM
From: paper man	Respond to of 4891

See last statment. second version edit <Reuters edit> Study sheds new light on how HIV infects cells By Patricia Reaney LONDON, Aug 18 (Reuters) - Spanish researchers have discovered why the progression of the HIV virus that causes AIDS is delayed in some sufferers, which could provide a new approach to fighting the disease. HIV infects the body through receptors for chemokines -- signalling 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. ''Screening for molecules that bring together the chemokine receptors result in a new generation of compounds that might be extremely effective against HIV,'' said Martinez-A. 09:14 08-18-99 Copyright 1999 Reuters Limited. All rights reserved. Republication or redistribution of Reuters content, including by framing or similar means, is expressly prohibited without the prior written consent of Reuters. Reuters shall not be liable for any errors or delays in the content, or for any actions taken in reliance thereon.