Scientists at The Scripps Research Institute (TSRI) have found a way to tether HIV-fighting antibodies to immune cells, creating a cell population resistant to the virus. Their experiments under lab conditions show that these resistant cells can quickly replace diseased cells, potentially curing the disease in a person with HIV.
The study is published in the journal Proceedings of the National Academy of Sciences.
The researchers, led by study senior author Richard Lerner, M.D., Lita Annenberg Hazen Professor of Immunochemistry at TSRI, plan to collaborate with investigators at City of Hope’s Center for Gene Therapy to evaluate this new therapy in efficacy and safety tests, as required by federal regulations, prior to testing in patients.
“City of Hope currently has active clinical trials of gene therapy for AIDS using blood stem cell transplantation, and this experience will be applied to the task of bringing this discovery to the clinic,” said John A. Zaia, M.D., director of the Center for Gene Therapy in the Hematological Malignancy and Stem Cell Transplantation Institute at City of Hope. “The goal will be the control of HIV in patients with AIDS without the need for other medications.”
“We at TSRI are honored to be able to collaborate with physicians and scientists at City of Hope, whose expertise in transplantation in HIV patients should hopefully allow this therapy to be used in people,” added Lerner.
The new TSRI technique offers a significant advantage over therapies where antibodies float freely in the bloodstream at a relatively low concentration. Instead, antibodies in the new study hang on to a cell’s surface, blocking HIV from accessing a crucial cell receptor and spreading infection.
Xie called it the “neighbor effect.” An antibody stuck nearby is more effective than having many antibodies floating throughout the bloodstream. “You don’t need to have so many molecules on one cell to be effective,” he said.
Before testing their system against HIV, the scientists used rhinovirus (responsible for many cases of the common cold) as a model. They used a vector called lentivirus to deliver a new gene to cultured human cells. This gene instructed cells to synthesize antibodies that bind with the human cell receptor (ICAM-1) that rhinovirus needs. With the antibodies monopolizing that site, the virus cannot enter the cell to spread infection.
“This is really a form of cellular vaccination,”
The new TSRI technique offers a significant advantage over therapies where antibodies float freely in the bloodstream at a relatively low concentration. Instead, antibodies in the new study hang on to a cell’s surface, blocking HIV from accessing a crucial cell receptor and spreading infection.
Xie called it the “neighbor effect.” An antibody stuck nearby is more effective than having many antibodies floating throughout the bloodstream. “You don’t need to have so many molecules on one cell to be effective,” he said.
Before testing their system against HIV, the scientists used rhinovirus (responsible for many cases of the common cold) as a model. They used a vector called lentivirus to deliver a new gene to cultured human cells. This gene instructed cells to synthesize antibodies that bind with the human cell receptor (ICAM-1) that rhinovirus needs. With the antibodies monopolizing that site, the virus cannot enter the cell to spread infection.