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Researchers at the University of Minnesota, the Howard Hughes Medical Institute and the University of Toronto have discovered a way to prevent the development of cancers linked to two viruses, including the virus that causes infectious mononucleosis – more commonly known as mononucleosis infectious. the "kisses disease" – which infects millions of people around the world each year.
Posted in Microbiology of nature, the research focuses on how the Epstein-Barr virus (EBV) and the herpes virus of Kaposi's Sarcoma Virus (KSHV) protect themselves from destruction in the human body.
"People infected with EBV or KSHV will have the virus for life," said Adam Cheng, a student in the Medical Scientist Training Program (MSTP) at the University of Minnesota's School of Medicine and lead author of the University of Minnesota. 39; study. "In most cases, the virus will remain dormant, however, these viruses can sometimes reactivate and cause abnormal growth of cancer cells, but as a result of our research, the data suggests that it may be be possible to remove the virus indefinitely. "
Under ideal conditions, a human DNA enzyme called APOBEC3B is able to mutate and kill EBV and KSHV viruses when it invades and replicates inside the body. However, researchers have found that both viruses are capable of producing defense proteins – BORF2 and ORF61, respectively – that bind directly to the APOBEC3B enzyme. In doing so, APOBEC3B is unable to mutate and kill viral DNA and moves away from virus replication sites.
"Our work suggests that by blocking the virus's defense proteins, it would be possible to treat mono and prevent the development of cancers caused by EBV and KSHV," said Dr. 39 senior author Reuben Harris, Ph.D. "Viral defense proteins are excellent targets for drug development."
The researchers used CRISPR / Cas9-mediated genome engineering to suppress the EBV defense protein. Through this process, the human APOBEC3B enzyme has been able to mutate the virus, rendering it harmless and unable to replicate in cells.
"We are already working hard to extend these cell results to mice and other complex organisms," Harris said. "The preliminary data is very promising and we hope to make great progress in future studies."
"This is an excellent example of how an unbiased fundamental scientific experience can create new therapeutic opportunities." We could not have anticipated such an unusual role of BORF2 in inhibiting APOBEC3B and the protection of EBV genomes, "said Lori Frappier, Ph.D. author of the study and professor at the University of Toronto.
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Material provided by University of Minnesota. Note: Content can be changed for style and length.
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