An image of hepatitis C Image Source: MIT
Drug Discovery & Development - February 02, 2012
Researchers from Massachusetts Institute of Technology (MIT), Rockefeller University, and the Medical College of Wisconsin have developed a way to establish a hepatitis infection in liver-like cells from induced pluripotent stem cells (iPSCs), enabling scientists to study how genetic differences produce varying responses in patients infected with hepatitis C.
Sangeeta Bhatia, a professor of health sciences, technology and electrical engineering, and computer science at MIT and Charles Rice, a professor of virology at Rockefeller University, reported that they could induce liver cells to grow outside the body by growing them on micropatterned plates that direct their organization. The liver cells can be infected with hepatitis C, but they cannot be used to proactively study the role of genetic variation in viral responses because they come from organs that have been donated for transplantation and represent only a small population.
To make cells with more genetic variation, Bhatia and Rice teamed up with Stephen Duncan, a professor of human and molecular genetics at the Medical College of Wisconsin who showed he could transform iPSCs into liver-like cells.
MIT postdoc Robert Schwartz and graduate student Kartik Trehan took the liver-like cells and infected them with hepatitis C. To confirm that infection had occurred, the researchers engineered the viruses to secrete a light-producing protein every time they went through their life cycle.
The researchers’ goal is to take cells from patients who had unusual reactions to hepatitis C infections, transform those cells into liver cells, and study their genetics to see why they responded the way they did. “Hepatitis C virus causes an unusually robust infection in some people, while others are very good at clearing it. It’s not yet known why those differences exist,” Bhatia says.
One potential explanation is genetic differences in the expression of immune molecules such as interleukin-28, a protein that has been shown to play a role in the response to the hepatitis infection. Other possible factors include cells’ expression of surface proteins that enable the virus to enter the cells, and cells’ susceptibility to having viruses take over their replication machinery, and other cellular structures.
The research was published in the Proceedings of the National Academy of Sciences.
Release Date: Feb. 1, 2012
Source: Massachusetts Institute of Technology
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