Researchers from Temple University and UNMC collaborate in a study recently published in the journal Proceedings of the National Academy of Sciences. Gene-editing therapy targeting both HIV-1, the virus responsible for AIDS, and CCR5, the co-receptor assisting viral entry into cells, has been de
Human Immunodeficiency Virus is a virus that attacks the immune system, making it difficult for the body to fight off infections and diseases. HIV is primarily transmitted through sexual contact, sharing of needles, or from mother to child during pregnancy, childbirth, or breastfeeding. If left untreated, HIV can progress to acquired immunodeficiency syndrome , which can be fatal.
“We are true partners, and what we achieved here is really spectacular,” Dr. Gendelman said. “Dr. Khalili’s team generated the essential gene-editing constructs, and we then applied those constructs in our LASER-ART mouse model at Nebraska, figuring out when to administer gene-editing therapy and carrying out analyses to maximize HIV-1 excision, CCR5 inactivation, and suppression of viral growth.”
To prevent rebound infection, Dr. Khalili and colleagues began work on next-generation CRISPR technology for HIV excision, developing a new, dual system aimed at permanently eliminating HIV from the animal model. “From success stories of human HIV patients who have undergone bone marrow transplantation for leukemia and been cured of HIV, our hypothesis was that the loss of the virus’s receptor, CCR5, is important to permanently eliminating HIV infection,” he explained.
The new dual CRISPR gene-editing strategy holds exceptional promise for treating HIV in humans. “It is a simple and relatively inexpensive approach,” Dr. Khalili noted. “The type of bone marrow transplant that has brought about cures in humans is reserved for patients who also have leukemia. It requires multiple rounds of radiation and is not applicable in resource-limited regions, where HIV infection tends to be most common.
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