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A new strategy to fight HIV and AIDS

An international team of researchers has developed a novel strategy against HIV. They added two genes to immune cells which 'transformed them into potent weapons that destroy cells infected with HIV, the virus that causes AIDS.' This idea of 'genetically engineering immune cells to redirect their infection-fighting ability toward killing HIV-infected cells could lead to an entirely new approach for combating AIDS.' This research looks promising, but it's only working in labs right now. But read more...
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Written by Roland Piquepaille, Inactive on

An international team of researchers has developed a novel strategy against HIV. They added two genes to immune cells which 'transformed them into potent weapons that destroy cells infected with HIV, the virus that causes AIDS.' This idea of 'genetically engineering immune cells to redirect their infection-fighting ability toward killing HIV-infected cells could lead to an entirely new approach for combating AIDS.' This research looks promising, but it's only working in labs right now. But read more...

This research project has been led by Dr. Harris Goldstein, Director of the Einstein/MMC Center for AIDS Research (CFAR). Here is a link to his research objectives. But Goldstein was not alone to work on this study. There were other Einstein researchers involved as well as scientists and doctors of Harvard Medical School, the VU University Medical Center of Amsterdam, in the Netherlands, and St. Jude Children's Hospital in Memphis, Tennessee.

Before going further, here is how HIV works. "After infecting a cell, HIV instructs it to make viral proteins. Tiny bits of these proteins, known as peptides, are displayed on the surface of the infected cell—the cell's way of signaling the immune system that it is infected. Detecting virus-infected cells so they can then be eliminated is the job of CTLs and the protein molecules, known as T-cell receptors, that jut from their surface. If a CTL's T-cell receptor has the right amino acid sequence, it will recognize the HIV peptide on the infected cell as foreign -- prompting the CTL to multiply and attack the infected cell. But all too often, this battle between activated CTLs and HIV-infected cells ends badly. Why, then, are super CTLs of elite controllers so effective in killing HIV-infected cells?"

After searching an answer to this question, the researchers decided to 'reprogram' these CTLs by inserting specific genes into their chromosomes. "'We demonstrated that these genetically reprogrammed CTLs have very strong activity in terms of killing HIV-infected cells in both test tubes and an animal model,' says Dr. Goldstein. In some of the animal studies, for example, the researchers injected mice with both HIV-infected human cells and with reprogrammed naïve CTLs into which the HIV-recognizing T-cell receptor genes had been inserted using the lentiviral delivery system. One week later, when the researchers looked for HIV-infected human cells in the animals, they found that the infected cells had virtually been eliminated."

If this technique works with animals, will it work for humans? Here are some Goldstein's ideas about the future. "'Ultimately, we'd like to remove CTLs from patients, convert them into potent HIV-specific CTLs by inserting a variety of HIV-specific CTL receptor genes, and then re-infuse these fresh, genetically reprogrammed CTLs back into patients. By reinforcing the immune system in this way, we hope to turn the tide of battle against HIV in favor of people infected with the virus.'"

In other words, even the lead researcher doesn't really know if this technique will work on people infected by HIV.

For more information, this research work has been published in The Journal of Virology under the very long title "Lentiviral Vectors Encoding Human Immunodeficiency Virus Type 1 (HIV-1)-Specific T-Cell Receptor Genes Efficiently Convert Peripheral Blood CD8 T Lymphocytes into Cytotoxic T Lymphocytes with Potent In Vitro and In Vivo HIV-1-Specific Inhibitory Activity" (Volume 82, Issue 6, Pages 3078-3089, March 2008). Here is a link to the abstract which is undertandable only by experts in the field.

Sources: Albert Einstein College of Medicine news release, March 4, 2008; and various websites

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