Jeff Habig


Research Scientist


B.A., Computer Science, Gustavus Adolphus College Ph.D., Cancer Biology, University of Wisconsin - Madison Postdoctoral fellowship, Howard Hughes Medical Institute, University of Utah


After working as a computer scientist, Dr. Habig obtained his Ph.D. at the University of Wisconsin research aimed at understanding how cancer-causing hepatitis B virus (HBV) replicates its genome through reverse transcription in the liver of infected individuals. Since then, he has researched the mechanism of RNA interference in C. elegans to better understand cellular defense against viral infection.


Habig, J.W., P.J. Aruscavage, and B.L. Bass (2008). In C. elegans, high levels of dsRNA allow RNAi in the absence of RDE-4. PLoS ONE, 3(12):e4052.

Welker, N., J.W. Habig, and B.L. Bass (2007). Genes misregulated in C. elegans deficient in Dicer, RDE-4 or RDE-1, are enriched for innate immunity genes. RNA, 13:1-13.

Habig, J.W., T. Dale, and B.L. Bass (2007). miRNA Editing – We Should Have Inosine This Coming. Molecular Cell, 25:792-793.

Habig, J.W. and D.D. Loeb (2006). Sequence identity of the direct repeats, DR1 and DR2, contributes to the discrimination between primer translocation and in situ priming during replication of duck hepatitis B virus. Journal of Molecular Biology, 364(1):32-43.

Habig, J.W. and D.D. Loeb (2003). Template switches during plus-strand DNA synthesis of duck hepatitis B virus are influenced by the base composition of the minus-strand terminal redundancy. Journal of Virology, 77:12412-20.

Habig, J.W. and D.D. Loeb (2003). The conformation of the 3’ end of the minus-strand DNA makes multiple contributions to template switches during plus-strand DNA synthesis of duck hepatitis B virus. Journal of Virology, 77:12401-11.

Habig, J.W. and D.D. Loeb (2002). Small DNA hairpin negatively regulates in situ priming during duck hepatitis B virus reverse transcription. Journal of Virology, 76:980-9.

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