Brian Krueger is the owner, creator and coder of LabSpaces by night and Next Generation Sequencer by day. He is currently the Director of Genomic Analysis and Technical Operations for the Institute for Genomic Medicine at Columbia University Medical Center. In his blog you will find articles about technology, molecular biology, and editorial comments on the current state of science on the internet.
My posts are presented as opinion and commentary and do not represent the views of LabSpaces Productions, LLC, my employer, or my educational institution.
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In the current political climate it has become clear that science is a major target of Republican directed budget cuts. However, the soundbytes of politics do not represent the importance of science in our lives. Because of this, I think it's extremely important that we explain why some of our model systems are so important for understanding how viruses and ultimately human disease work.
In the lab that I run, we currently work on mutating two different herpesviruses. One of these is Kaposi's Sarcoma Herpesvirus (KSHV) and the other is Murid Herpesvirus 68 (MHV68). Both of these viruses are gammaherpesviruses. In humans, KSHV only really ever becomes a problem in individuals who have a compromised immune system such as those infected with human immunodeficiency virus (HIV). KSHV is an interesting virus because its default program is latency, meaning that once it gets into your cells, it turns itself off and waits for conditions which allow it to grow and take over. This is akin to a bear hibernating in the winter. We do not understand how or why this virus defaults to the latency program, and it is the topic of intense ongoing research. Additionally, understanding how the virus transitions from its latent state (hibernating) and switching to its lytic state (crazed, angry, killer mother bear) is extremely important in trying to understand how to get the upperhand on this virus. We know that cellular stress plays a role in this process, but the exact events that happen within the cell that make this occur are unknown. We can artificially cause the virus to switch states by really pissing off the cells, but as virologists we are more interested in how this happens in a more natural setting. Now, we can do a lot of experiments in cells, but this doesn't give us the full picture on how the virus affects the biology of the host. Unfortunately, KSHV only infects humans or primates. Doing controlled experiments in humans with this virus are either too hard or extremely unethical and doing experiments in monkeys is very expensive. This is where MHV68 comes in! Fortunately, MHV68 is very closely related to KSHV so we can use MHV68 in mice to provide information on how a natural KSHV infection might occur in humans without the increased cost of using KSHV infected primates.
In science, MHV68 would be considered a model system. We use model systems a lot in science because doing experiments on humans is very expensive. We do the ground work in cheaper animals before we use our findings to help treat human disease. Other very important model systems in biology include fruit flies, flat worms, yeast, e. coli bacteria, zebrafish, and xenopus frogs. If in the future you hear a politician making blanket statements about scientists' researching X in Y, take a minute to try to understand what is actually being said. It's likely that these statements are made out of context and don't accurately represent the importance of the research being conducted.
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