Stanley M Lemon, MDStanley M Lemon, MD
Adjunct Professor, Microbiology & Immunology and Internal Medicine
Molecular mechanisms involved with replication of positive-strand RNA viruses and the pathogenesis of human hepatitis viruses, particularly hepatitis C virus; antiviral drug development; mechanisms of immune evasion of hepatitis C virus

Email: smlemon@utmb.edu

Education: MD, 1972, University of Rochester School of Medicine and Dentistry, New York
AB, 1968, Princeton University, Princeton, New Jersey

Research Interests

The research in the Lemon lab focuses on the molecular pathogenesis of hepatitis C. Dr. Lemon's research group is defining the structure of the RNA segments that control the initiation of translation as well as those recognized by the replicase complex to initiate viral RNA synthesis. His group is, thus, dissecting the mechanisms of hepatitis C virus RNA replication, and the process of infectious particle assembly. Toward that end, they have developed robust, cell-culture based hepatitis C virus RNA and, more recently, virus replication systems, that allow structure-function correlates to be studied using reverse molecular genetics. Dr. Lemon is also interested in mechanisms of hepatocellular injury in chronic hepatitis C. His research group has developed transgenic mouse models of hepatitis C-related liver injury, including hepatocellular carcinoma, and constructed hepatoma-derived and other cell lines with conditional expression of hepatitis C virus proteins. They are using these cells and their infectious virus systems to study the effects of hepatitis C virus protein expression on post-transcriptional regulation of the retinoblastoma tumor suppressor protein and its effect on host cell proliferation and chromosomal stability. Dr. Lemon is also interested in the mechanisms by which hepatitis C virus evades intrahepatic innate cellular immune defenses. His group has shown that the NS3/4A serine protease directs the cleavage of a key Toll-like receptor adaptor protein, TRIF, resulting in an effective blockade of dsRNA-induced activation of the transcription factors interferon regulatory factor 3 (IRF-3) and NK-kB and their cognate gene targets. The protease recognizes TRIF through a unique molecular interaction that differs from its recognition of natural viral polyprotein substrates, and also cleaves IPS-1, a recently recognized signaling protein, thereby disrupting a second, TRIF-independent pathway leading to interferon synthesis that is initiated by and dependent upon the cellular DExH(D) RNA helicase, RIG-I. The Lemon lab interacts closely with on- and off-campus collaborators in studying interactions of hepatitis C virus with the innate immune system investigating the role of hepatitis C core protein expression in mitochondrial injury in hepatitis C and in the construction and evaluation of inducible transgenic mouse models in which cellular responses to hepatitis C virus proteins can be studied.

Recent Publications

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