Zika virus has a clever strategy, reports Los Angeles’ ANI on September 13. In order to mount an effective immune response, the body’s dendritic cells are where viruses first make their way after infection. “Dendritic cells are essential cells of the innate immune system,” says LJI Professor Sujan Shresta, Ph.D., a member of the LJI Center for Infectious Disease and Vaccine Research.
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In the words of Aaron Carlin, M.D., Ph.D., co-leader of the current work and former research assistant in the Shresta Lab, “knowing how viruses interact with human cells is vital for understanding how to cure or prevent infection in the future.” Former LJI postdoctoral researcher Emilie Branche, Ph.D., developed a model to investigate the mechanisms through which dengue and zika viruses infect dendritic cells. She performed experiments on human immune cells called monocytes, causing them to differentiate into dendritic cells.
Branche looked into the ways in which gene expression altered in these dendritic cells following exposure to either dengue or zika. Then, she compared the changes in gene expression to those seen in cells that had undergone a “mock infection,” providing a detailed look at how Zika takes over host cells.
Experts have shown that the Zika virus interferes with genes in dendritic cells responsible for lipid metabolism. The virus triggers an increase in lipid (fat molecule) production by activating a cellular protein called SREBP. New Zika virus copies, intended to spread infection throughout the body, were produced using these lipids as building blocks.
We showed that Zika, but not dengue, alters cellular metabolism to facilitate replication,” says Branche.
Afterward, they looked into whether Zika causes more cells to become lipid manufacturers. Although Zika is also known to target brain precursor cells, the study team showed that Zika does not affect genes involved in lipid metabolism in these cells. It came as a surprise to Shrestha that these changes only affected dendritic cells and that Zika, unlike dengue, altered lipid production.
According to Shrestha, “These viruses are wild,” meaning that their ability to change host cell responses varies greatly depending on the virus and the cell type in question. The next step is to design antivirals that block Zika from using its lipid metabolism-related genes. Therapeutic suppression of SREBP has promise, according to the most recent research.
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How Should We Handle Dengue, a Close Relative of Zika?
Shrestha believes that, due to the similarities amongst flaviviruses, a “cocktail” of inhibitors will be necessary to effectively treat various diseases. One such inhibitor is selective for sigma receptor-interacting protein beta. There will be more discoveries made about these viruses, she says, the closer we get to a “pan-flavivirus” inhibitor. (ANI)
The ANI news service automatically generated this report. ThePrint disclaims all liability for its accuracy.
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