Recorded: 06 Jun 2006
We learned something new about an old world, that’s what I would state. There were leftovers from the very early days and there were apparently some very general mechanisms to break genomes or genes, to cleave them and get rid of them, and these were very ancient antiviral mechanisms. So, the similarity comes that how do you get rid of a virus and the defense mechanisms have evolved after our immune system now in the millions and we have a very broad spectrum of how can a cell perform an antiviral defense, and that was the topic of this meeting. And for me personally, the exciting part of it was many years back I found this Ribonuclease H as a member of the retroviruses and this is an enzyme-cleaving RNA and RNA-DNA hybrids. Now, when they looked at the cleavage-enzyme doing all of this SI, what they call it silencing of RNA, by double stranded RNA, this RNase H structured enzyme. So, I was asking myself if the structure is like an RNase H, it doesn’t cleave RNA-DNA hybrids, but double stranded RNA, is there any relationship. So, looking at the RNase H of this ionery machinery and of retrovirus machinery. I want to make the story simple; my vision is of my concept is, the replication machinery of retroviruses, including several gene components in highly related to the antiviral defense machinery of the SI machinery that goes probably several of the enzymes have evolved taking over some of the same function. Now you ask, who learned from whom, probably from both side mutually and that’s how the virus evolves and how the cell evolves. So I think there is a cross-talk between the two of them and one of the cross-talk enzymes is the RNase H.
Yeah, but the particular kind of information you learn from this small RNA world – that’s new. The plant people knew about it much earlier, you see. The plant papers from 1928 or something, they knew what was going on. Molecular biology had to be enough developed to know what, to understand the mechanisms and for the virologist it’s interesting to see how the virus is attacked, by an antiviral defense, and how it fights back. So, what are the mechanisms a virus develops to defend itself against the secondary defense mechanism. So that teaches us a lot.
Karin Moelling currently retired professor, still affiliated with the University of Zurich and the Max-Planck-Institute for Molecular Genetics in Berlin. She studied molecular biology at the University of Berkely, Califonia. She received her PhD at the Max-Planck-Institute for Virology at Tübingen in Germany. She did two post-doctoral research at the Robert Koch Institute in Berlin (1973-1975), and at the Institute of Virology, University Giessen. In 1977 she received her Habilitation at the University of Giessen in Biophysics on "Replication of retroviruses".
From 1976 till 1981 she was the Head of Independent Research Group at Max-Planck-Institute for Molecular Genetics in Berlin, Germany, on oncogenes, proto-oncogenes, cancer and HIV. In 1993 she became the Director of Institute of Medical Virology (IMV) and Full Professor at University of Zurich in Switzerland, she held this position till 2008. Between 2008-2009 she was Fellow of Institute of Advanced Study in Berlin and between 2008-2011 she became a Group Leader, Viruses and Cancer at University of Zurich.
Her research focus on retroviruses and cancer from molecular mechanisms to drug design. She is a Member of the European Molecular Biology Organization. She received several awards e.g. SwissAward in 2007, 4 prices: Czerny Price, Richtzenhain Price, Meyenburg Price and Ansman Price. She was Selected as Heisenberg Fellow in German Science Foundation.