Important note: Information in this article was accurate in 1997. The state of the art may have changed since the publication date.

Reuters NewMedia, Inc. - Thursday November 20, 7:37 pm Eastern Time
Maggie Fox, Health and Science Correspondent

Very early treatment with a cocktail of drugs known to control the virus could give the immune system just the break it needs to effectively battle the infection, they said.

The secret may lie in the clues the immune system uses to recognize HIV, Dr. Bruce Walker and colleagues at Massachusetts General Hospital said.

All bacteria, viruses and other invaders have a protein coat that the body's immune system can recognize. Researchers use this when they try to formulate vaccines, and have tried a number of proteins from HIV's coat.

Just like a bloodhound, if the immune system cells known as T-cells can be given HIV proteins to smell once, they can remember that "smell" and chase invaders down -- or so the theory goes.

Unfortunately, HIV infects the very T-cells that fight infection, so when they show up on the scene, instead of taking down the suspect they are themselves captured.

Walker's team found that the cells evade infection better when they concentrate on one of HIV's proteins, known as p24.

"One of the biggest mysteries in our understanding of AIDS and HIV has been why the immune responses that usually control viral infections don't work," Walker said in a statement.

"Our work now suggests a simple explanation for how HIV escapes the normal immune response, why the immune system slowly but inexorably breaks down, and why a very small group of people have been able to avoid getting sick from this virus."

Walker's team worked with a hemophiliac who had been infected via a blood transfusion 18 years ago, but who had virtually no evidence of HIV in his blood. He had never been ill and his body showed a strong antibody response to the virus -- indicating it was keeping the HIV in check.

His CD4 T-cells -- also known as helper T-cells -- reacted specifically to p24. "Not only did this individual have HIV-specific helper cells, but he had a huge helper-cell response, the first such response we had ever seen to HIV," Walker said.

They then found 10 HIV infected people who had not yet taken any AIDS drugs.

Checking their blood, they found that how well their immune systems responded to p24 was a good indicator of how bad their infection was. "Individuals with the strongest p24-specific proliferative response had the lowest viral loads," they wrote in a report in the journal Science.

"Those individuals with higher HIV viral loads had a markedly decreased ability to respond to p24," they wrote.

The p24 protein seemed to be the key, and the researches confirmed that in a study in a second group of 15 infected people from San Francisco.

They said this could mean the body only rarely generated the right kind of T-cells in response to HIV infection.

"We began to develop a theory about why these virus-specific cells usually don't appear in HIV-infected people," Dr. Eric Rosenberg, who led the study, said.

"Perhaps the very helper cells capable of recognizing HIV were being destroyed in the earliest stage of infection. We wondered if antiviral treatment at that time might keep these helper cells from being eliminated."

They tested this idea in a patient who had just been infected days before. Sure enough, when he got strong drugs, the amount of virus in his bloodstream -- viral load -- dropped, and his T-cells showed the specific p24 response.

"This suggests that there is a window of time -- and we don't know yet how large it is -- during which we might be able to salvage the helper T-cell response through vigorous antiviral treatment," Walker said.

"So it could be critically important for physicians to be alert for the symptoms of acute (early) HIV infection, and in those patients who appear to be at risk, to test for the presence of the virus."

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