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Mount Sinai researchers develop first successful laboratory model for studying hepatitis C
Date:8/2/2013

ing macaque cells to initiate infection compared to human cells because changes in the macaque form of a certain cell surface receptor rendered it less functional than the human version. This cell entry block could be overcome by expressing the human version of this receptor in macaque cells. Furthermore, HCV infection of normal macaque cells was greatly enhanced by changes to the virus that loosened its requirements for that receptor.

"Our discovery shows that by manipulating either host or viral genetics we can efficiently infect macaque cells," said Dr. Evans. "These findings may open doors for the field of HCV research, lead to new animal models, and hopefully vaccines and therapies."

Next, Dr. Evans plans to take these experiments out of petri dishes by attempting to infect macaques in vivo with the mutant HCV that can use the receptors this animal naturally expresses. If successful, this work would provide a new, much-needed animal model for HCV studies and vaccine development.


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