Matthew J Evans, PhD

The Evans Lab studies how hosts and viruses interact, with a focus on the hepatitis C virus (HCV). HCV is responsible for more than half of liver cancers in the Western Hemisphere. While therapies to treat HCV are improving, these drugs will not be available to all patients. Thus further study of this virus is warranted for both therapeutic and vaccine design.  One aim of the Evans Lab is to understand how this virus enters host cells. Using a novel HCV permissive polarized cell system, we found that tight junction proteins that we identified as critical to HCV cell entry are used late in this process. We are currently exploring how virion translocation to tight junctions occurs and endocytic signals within tight junction proteins are responsible for virion internalization.

We also study how a liver specific microRNA, miR-122, influences HCV replication and tropism. By modulating miR-122 expression, we created a new cell system that exhibits authentic innate immune responses to HCV infection. We also showed the HCV genetics influences response to miR-122 inhibitors that are currently in clinical development.

Another aim of the Evans Lab is to determine how host differences impact the tight HCV species tropism. By recently showing that pigtail macaques support persistent HCV infection in vivo, we have established the only available immunocompent HCV animal model that will be essential for HCV pathogenesis and vaccine studies. We are further characterizing macaque HCV infections, including how the virus changes during infection and how the host immune system responds.

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