Dr. Lemon’s research interests focus on the
molecular pathogenesis of viral hepatitis caused by the positive-strand RNA viruses responsible
for hepatitis C and hepatitis A. Although these agents represent different virus families, they
share a general strategy for their replication as well as several specific features of the
viral life cycle. Both viruses initiate the 5' cap-independent translation of their protein
complement by a process of internal ribosome entry on the positive-strand viral RNA. Dr.
Lemon’s laboratory is interested in defining the structure of the RNA segments that control the
initiation of translation, and in developing a better understanding of the mechanisms by which
this process occurs. The ultimate aim is to exploit the internal ribosome entry site (IRES) as
a target for antiviral intervention, or to manipulate it in a way that may attenuate the
pathogenic potential of the virus for vaccine purposes. On a broader scale, the laboratory is
engaged in efforts to expand the repertoire of laboratory systems available for the study of
hepatitis C virus. This includes the development of alternative model systems for hepatitis C,
including the development and characterization of hepatitis C transgenic mice. Transgenic mice
expressing various hepatitis C proteinshave been developed in the laboratory, and have been
shown to be at risk for hepatic steatosis and hepatocellular carcinoma. State-of-the-art gene
chip techniques are being used in an effort to understand the molecular basis of these
phenotypes. Other research efforts include the construction and evaluation of infectious cDNA
copies of the hepatitis C genome, and the evaluation of other flaviviruses (e.g., GB virus B)
as surrogate laboratory models for hepatitis C. The laboratory interacts widely with a number
of basic and clinical scientists at UTMB who share the desire to develop better ways to control
this common and potentially life-threatening infection. |