Protein Protects Cells From HIV Infection
Researchers from the NYU Langone Medical Center are making progress in the fight against HIV after learning how some cells in the body repel the HIV virus by starving and retarding its growth.
Research co-leader, Nathaniel R. Landau, PhD., explained that their discovery could pave the way for new therapeutic research at halting or slowing the HIV’s progression to AIDS. “A lot of research on viruses, especially HIV, is aimed at trying to understand what the body’s mechanisms of resistance are and then to understand how the virus has gotten around these mechanisms,” Landau said in a Monday press release.
Dendritic cells containing the SAMHD1 protein are resistant to infection from HIV, Landau and his team discovered. They set out to find out why and how SAMHD1 protects such cells and hoped to find a way of synthetically applying this same protection to other cells in the body.
SAMHD1 lowered the levels of deoxynucleoside triphosphates (dNTPs) below that needed to build viral DNA and prevented infection. When removed, the SAMHD1 cells had higher levels of dNTPs and were infected by HIV.
“By depleting the pool of available dNTPs, SAMHD1 effectively starves the virus of a building block that is central to its replication strategy,” the study says. It is possible for macrophages and dendritic cells to produce SAMHD1 as they are “mature cells” which do not go on to produce new cells.
Baek Kim, professor and researcher from the University of Rochester Medical Center, explained to BBC’s James Gallagher: “It makes sense that a mechanism like this is active in macrophages. Macrophages literally eat up dangerous organisms, and you don’t want those organisms to have available the cellular machinery needed to replicate and macrophages themselves don’t need it, because they don’t replicate.”
“So macrophages have SAMHD1 to get rid of the raw material those organisms need to copy themselves. It’s a great host defense.”
Scientists are excited to explore and fully understand how SAMHD1 protects cells and look forward to eventually coming up with novel ways to stop HIV’s ability to spread, reports Medical News Today.
Dr. Landau concluded: “Over the past few years, a number of these natural resistance mechanisms have been identified, specifically in HIV, but some have potential applications to other viruses, as well. This is a very exciting time in HIV research.”
“Many of the virus’ secrets are being revealed through molecular biology, and we’re learning a tremendous amount about how our immune system works through the study of HIV.”
The results of the study are published in Nature Immunology.
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