Making a slight modification to a key liver cell protein in mice has taken scientists a step closer to developing a successful mouse model in which to study hepatitis C virus (HCV). Such a model is greatly needed to facilitate research into a vaccine for the virus.
Currently, mice can be infected with HCV if the animals are genetically engineered to produce human proteins that permit the virus to enter liver cells. However, HCV cannot replicate in the liver cells of such mice unless the virus’s genome has been altered or the animal’s immune system is suppressed.
Publishing their findings in the journal eLife, researchers in the new study zeroed in on whether a protein known as cyclophilin A is responsible for mouse liver cells’ resistance to infection with HCV. Humans require this protein for the virus to replicate in their liver cells. The investigators found that the mouse version of the protein was a lot less efficient at promoting HCV replication than the human cyclophilin A.
The investigators found that mutating the mouse version of cyclophilin A to more closely resemble the human version facilitated HCV replication in mouse liver cells.
However, when the scientists tested different versions of cyclophilin A in mouse liver cells that also contained a handful of other proteins required for HCV to enter cells and replicate, they found replication was still considerably lower than that seen in human cells. This finding suggests that more research is needed to develop more modifications that will boost HCV replication in mouse cells on par with what is seen in human cells.
To read a press release about the study, click here.
To read the study, click here.